Vasopressors Flashcards

1
Q
  1. Name the mechanisms of hypotension.
A
decreased HR
decreased preload
decreased contractility
decreased afterload/ vasodilation
decreased CO
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2
Q
  1. Describe the mechanism of hypotension: decreased HR
A

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

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3
Q
  1. Describe the mechanism of hypotension: decreased contractilty
A

decreased B1 stimulation, decrease in cAMP, decreased protein kinase, decreased Ca2+ influx

increased parasympt input

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4
Q
  1. Describe the mechanism of hypotension: vasodilation
A

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

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5
Q
  1. Know the hemodynamic monitoring methods: HR, preload, contractility, afterload and BP
A

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

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6
Q
  1. Understand risks of central line placement.
A

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

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7
Q
  1. Understand cardiac output measurement and SVR calculation.
A

MAP = COx SVR (SVR= afterload)

CO=HR x SV (SV= preload x contractility= EDV-ESV)

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8
Q
  1. Understand the mechanisms of action of (vasopressors and) inotropes.
A

inotropes: increase CO via increases in SV without changing HR

ideally without SE of dysrhythmias and vasoconstriction

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9
Q
  1. Synthetic noncatecholamines (vasopressor only) (3).
A

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

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10
Q
  1. Endogenous catecholamines (3).
A

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

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11
Q
  1. Synthetic catecholamines. (3)
A

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

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12
Q
  1. Noncatecholamine nonglycoside cardiac inotropic agents (inodilators).
A

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

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13
Q
  1. Cardiac glycoside: digoxin
A

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

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14
Q
  1. Ionized calcium
A

calcium chloride or Ca gluconate: increased contractility, CO and decreased HR and SVR

causes venous irritation/skin necrosis (CaCl)

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