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Anesthesia Pharm Midterm 2 > Maintaining Hemodynamic Stability: Vasopressor & Inotropes > Flashcards

Maintaining Hemodynamic Stability: Vasopressor & Inotropes Flashcards

1
Q

Bottom Line

A

anesthesia drugs cause hypotension and surgical stimulation causes hypertension- delicate balance
-our GOAL is to maintain organ and tissue perfusion (flow) and avoid hypertensive crisis

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2
Q

MAP=

A 
MAP= CO x TPR
MAP= CO X SVR
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3
Q

Flow=

A

Q= pressure/resistance

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4
Q

Cardiac Output=

A

CO= HR x SV

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5
Q

Stroke Volume=

A

SV= EDV-ESV

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6
Q

Hemodynamic Effects of Volatiles

A
  • dose dependent arterial hypotension:
  • -decreased LV afterload= decreased SVR & wall tension
  • -decreased myocardial contractility= negative inotrope (cardioprotective)
  • -left ventricular- arterial coupling= negative dromotrope
  • -depression of SA node= negative chronotrope (des is exception, tachycardia with rapid increase in dose)
  • -depress baroreceptor reflex control of arterial pressure to varying degrees (more so w/ older volatiles, Iso has the least effect)
  • SO, CO is more easily maintained as baroreceptor reflex compensates for decreased SVR and contractility
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7
Q

Nitrous Hemodynamic Effects

A

Nitrous causes direct negative inotropic effects

  • does not substantially affect left ventricular diastolic function
  • produces modest increases in pulmonary and systemic arterial pressure via a sympathomimetic effect
  • these actions are dependent to some degree on the baseline anestheticc
  • —-findings suggested that nitrous oxide does not alter sympathetic vasoconstrictor-induced maintenance of arterial pressure, which may be partially responsible for the relative stability of hemodynamics during nitrous oxide anesthesia
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8
Q

How low is too low of a decrease in BP in a healthy patient?

A

20-30% below baseline in normal healthy patient is OKAY

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9
Q

What patients should not be subjected to hypotension?

A
  • patients with known carotid stenosis, known valvular disorders, known heart failure, known fixed cardiac output, and known severe contrary artery stenosis.
  • these patients may develop cerebral or myocardial ischemia
  • maintain these patients at their normal BP*
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10
Q

BP and patients in the sitting position

A
  • patients in semi-reclining or sitting positions are at increased risk
  • always remember that the blood pressure decreases 2 mmHg for every 2.5 cm (1 in) height above the point of measurement
  • so blood pressure within the brain in a sitting patient under anesthesia is about 12-16 mmHg lower than that measured at the upper arm
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11
Q

What is a safe BP for patients in healthy adults undergoing anesthesia?

A

-a safe BP for patients without any conditions is to keep the blood pressure at a level equal to, or higher than 2/3 of the known resting mean arterial blood pressure (MAP)

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12
Q

Blood Pressure Control: Intrinsic Factors

A
  1. Frank Starling Mechanism (SV): maintain optium preload

2. SA and AV node (HR and AV synchronization): antiarrythmics

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13
Q

Blood Pressure Control: Nervous System

A
  1. Sympathetic (sympathomimetics)

2. Parasympathetics (anticholingerics, cholingerics)

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14
Q

Blood Pressure Control: Reflexes

A
  1. Baroreceptor: be aware of bradycardia w/ pure alpha agonists
  2. Chemoreceptor: maintain optimal oxygen sat, ETCO2, pH)
  3. Atrial receptor: bainbridge- maintain optimum pre-load
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15
Q

Blood Pressure Control: Humoral Factors

A

Renin-Angiotensin-Aldosterone System (vasopressin)

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16
Q

Baroreceptors

A
  • A sudden increase in BP leads to a decrease in HR, CO, and SVR
  • A sudden decrease in BP leads to increase in HR, Co, and SVR
  • when giving a pure alpha agonist you will see a decrease in HR due to this reflex
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17
Q

Vasopressin

A

-one 40 unit dose may be substituted for either first or 2nd dose of epi in cardiac arrest
-elimination half life is 10-20 minutes
-infusion rate 0.01-0.04 units/min
-may give 1-2 u boluses
-consider in refractory hypotension (shock, hemorrhage) and patients with are on ACE inhibitors
low dose: fluid retention
high dose: vasoconstrictive effects

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18
Q

Alpha 2

A

-when activated, alpha 2 receptors inhibit NTM release from presynaptic neurons

19
Q

Parasympathetic neurons

A

Long Pre, Short post
Pre: Parasympathetic= Nicotinic receptor, ACH released
Post: Parasympathetic= Muscarinic receptor, ACH released on heart & vessels

20
Q

Sympathetic neurons

A

Short Pre, Long Post
Pre: Parasympathetic= Nicotinic receptor, ACH released
Post: Sympathetic= Beta, Alpha receptors. NE released on hearts & vessels

Post: Sympathetic= Muscarinic receptors, ACH released on sweat glands and vessels
Post: Sympathetic= D1 receptors, Dopamine released on renal vessels
Adrenals: Epi and NE released on heart & vessels

21
Q

MAO

A
  • monoamine oxidase

- deaminates Epi, NE, and dopamine

22
Q

COMT

A
  • catechol-O-methyl transferase

- causes methylation of catecholamines in extra neuronal tissue

23
Q

Alpha 1

A

Location: vascular smooth muscle (peripheral, renal and coronary circulation)

  • contraction of radial muscle (myDriasis)
  • increase secretion of salivary glands
  • bronchoconstriction
  • decrease insulin secretion
  • spinchter contraction of upper GI tract
  • glycogenolysis
  • abdominal blood vessels: constriction
  • sphincter contraction- bladder
24
Q

Beta 1

A

Location: heart

  • increase HR
  • increase conduction velocity
  • increase contractility
25
Q

Beta 2

A

Location: vascular smooth muscle

  • increase secretion of salivary glands
  • bronchodilation
  • increase insulin secretion
  • gluconeogenesis
  • dilation of abdominal blood vessels
  • bladder: detrusor relaxation
26
Q

When dopamine is administered what happens?

A

-activation of DA1 receptors causes vasodilation, whereas activation of DA2 receptors causes inhibition of release of norepi from storage granules

27
Q

Larger doses of dopamine cause what?

A

-activation alpha 1- alpha 2 adrenoceptors on the post junctional effector cells to cause vasoconstriction

28
Q

Alpha 1 Receptors

A
  • Post synaptic
  • located in smooth muscle throughout the body
  • Agonists: pupil dilation, bronchoconstriction, uterine contraction, vasoconstriction (increase SVR, increase after load)
29
Q

Alpha 2 receptors

A
  • Pre-synaptic nerve terminals, negative feedback loop that inhibits NE release
  • activation inhibits cAMP levels which decrease Ca++ entry into the neuronal terminal and limits release of NE
  • Activation= sedation in CNS, reduced sympathetic outflow and peripheral vasodilation
30
Q

Beta Receptors

A
  • NE and Epi are equipotent on B1 receptors
  • epi is more potent on B2 than NE
  • b2 relaxes smooth muscle
  • b3 found in gall bladder and adipose tissue. May play a role in lipolysis and brown fat thermogenesis
31
Q

Phenylephrine

A
  • non-catecholamine w/ predominantly alpha 1 agonist activity (direct alpha 1 agonist)
  • dose dependent vasoconstrictor used to increase BP due to vasodilator effects of anesthetic agents
  • REFLEX BRADYCARDIA
  • can cause pulmonary HTN
32
Q

Ephedrine

A
  • synthetic non-catecholamine indirect and direct acting alpha and beta agonist
  • works by increasing the release of NE at the synaptic junction and similar direct alpha and beta effects of epi
  • –increase in BP, HR, contractility and CO, bronchodilator
  • longer duration of action and less potent than epi
  • direct stimulation of CNS (may increase MAC)
  • can get tachyphylaxis– depleting stores
33
Q

Ephedrine dosing

A

Dose:
IV bolus 2.5 to 10 mg (pediatric 0.1 mg/kg)
IM/SQ 25-50 mg (onset may be 10-20 min)
available in 1 ml vials of 50 or 25 mg/cc
-dilute for IV administration
-tachyphylaxis (works indirectly)

34
Q

Epinephrine

A
  • endogenous catecholamine synthesized in adrenal medulla
  • principle treatment in anaphylaxis and cardiac arrest
  • consider in severe bronchospasm (also stabilizes mast cells) hypotension w/ bradycardia and/or low CO
  • used to prolong the effects of local anesthetics-causes vasoconstriction
  • low dose: affects beta
  • high dose: affects alpha
35
Q

Epinephrine Dosing

A

-0.05 to 1.0 mg IV push (1 mg code)
-0.3-0.5 mg (IV/IM) Anaphylaxis**
IV gtt: 0.1 to 1.0 mcg/kg/min (1 mg/250 ml, 4 mcg/ml)
-extravasation of epi at a peripheral IV site may produce significant tissue ischemia

36
Q

Phenyl dosing

A

Dose: smal IV boluses of 50-100 mcg (0.5-1.0 mcg/kg)
duration: short, approx. 15 minutes
infusion rate: 0.25-1.0 mcg/kg/min (increase pressure but may impede renal blood flow)
Available in 10 mg/ml vial. Must be diluted for use. Usually 100 mcg/ml

37
Q

Epinephrine comes in which increments?

A

grams: mililters

38
Q

Norepi

A

-direct alpha 1 stimulation w/ little beta 2 activity produces intense vasoconstriction
alpha 1= alpha 2, B1&raquo_space;» B2
-increased contractility. Increased after load and some reflexive bradycardia
-does NOT have the advantages of B2 stimulation, e.g. renal and Gi blood dilation
-extravasation can cause tissue necrosis

39
Q

Norepi bolus

A
  • may be bolus 0.1 mcg/kg (short duration)
  • infusion 2-20 mcg/min, or 0.01 to 3 mcg/kg/min (higher rates in septic shock)
  • comes in ampules of 4 mg/4ml
  • must be diluted
40
Q

Dopamine

A

-endogenous non-selective direct and indirect adrenergic and dopamingeric agonist which varies with dosage

41
Q

Dopamine dosing

A

Beta 1 effects: 2-10 mcg/kg/min
Alpha 1 effects: > 10 mcg/kg/min
Dopaminergic effects: 0.5-2 mcg/kg/min

42
Q

Inotropes (Beta Selective)

A

Isoproterenol (Isuprel)

  • potent beta 1 agonist, little effect on alpha
  • positive chornotrope & inotrope

Dobutamine

  • initially considered as beta 1 selective, but more complicated than that
  • positive inotrope over chronotrope when compared to isuprel, some alpha 1
43
Q

Inodilators

A

-Milrinone
phosphodiesterase type II inhibitor
non catecholamine inodilator
—-increased CO w/ reduction in arterial pressure, LVED, and pulmonary vascular resistance

Anesthesia Pharm Midterm 2 (8 decks)

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