Maintaining Hemodynamic Stability: Vasopressor & Inotropes Flashcards
Bottom Line
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
MAP=
MAP= CO x TPR MAP= CO X SVR
Flow=
Q= pressure/resistance
Cardiac Output=
CO= HR x SV
Stroke Volume=
SV= EDV-ESV
Hemodynamic Effects of Volatiles
- 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
Nitrous Hemodynamic Effects
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
How low is too low of a decrease in BP in a healthy patient?
20-30% below baseline in normal healthy patient is OKAY
What patients should not be subjected to hypotension?
- 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*
BP and patients in the sitting position
- 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
What is a safe BP for patients in healthy adults undergoing anesthesia?
-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)
Blood Pressure Control: Intrinsic Factors
- Frank Starling Mechanism (SV): maintain optium preload
2. SA and AV node (HR and AV synchronization): antiarrythmics
Blood Pressure Control: Nervous System
- Sympathetic (sympathomimetics)
2. Parasympathetics (anticholingerics, cholingerics)
Blood Pressure Control: Reflexes
- Baroreceptor: be aware of bradycardia w/ pure alpha agonists
- Chemoreceptor: maintain optimal oxygen sat, ETCO2, pH)
- Atrial receptor: bainbridge- maintain optimum pre-load
Blood Pressure Control: Humoral Factors
Renin-Angiotensin-Aldosterone System (vasopressin)
Baroreceptors
- 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
Vasopressin
-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
Alpha 2
-when activated, alpha 2 receptors inhibit NTM release from presynaptic neurons
Parasympathetic neurons
Long Pre, Short post
Pre: Parasympathetic= Nicotinic receptor, ACH released
Post: Parasympathetic= Muscarinic receptor, ACH released on heart & vessels
Sympathetic neurons
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
MAO
- monoamine oxidase
- deaminates Epi, NE, and dopamine
COMT
- catechol-O-methyl transferase
- causes methylation of catecholamines in extra neuronal tissue
Alpha 1
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
Beta 1
Location: heart
- increase HR
- increase conduction velocity
- increase contractility
Beta 2
Location: vascular smooth muscle
- increase secretion of salivary glands
- bronchodilation
- increase insulin secretion
- gluconeogenesis
- dilation of abdominal blood vessels
- bladder: detrusor relaxation
When dopamine is administered what happens?
-activation of DA1 receptors causes vasodilation, whereas activation of DA2 receptors causes inhibition of release of norepi from storage granules
Larger doses of dopamine cause what?
-activation alpha 1- alpha 2 adrenoceptors on the post junctional effector cells to cause vasoconstriction
Alpha 1 Receptors
- Post synaptic
- located in smooth muscle throughout the body
- Agonists: pupil dilation, bronchoconstriction, uterine contraction, vasoconstriction (increase SVR, increase after load)
Alpha 2 receptors
- 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
Beta Receptors
- 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
Phenylephrine
- 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
Ephedrine
- 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
Ephedrine dosing
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)
Epinephrine
- 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
Epinephrine Dosing
-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
Phenyl dosing
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
Epinephrine comes in which increments?
grams: mililters
Norepi
-direct alpha 1 stimulation w/ little beta 2 activity produces intense vasoconstriction
alpha 1= alpha 2, B1»_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
Norepi bolus
- 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
Dopamine
-endogenous non-selective direct and indirect adrenergic and dopamingeric agonist which varies with dosage
Dopamine dosing
Beta 1 effects: 2-10 mcg/kg/min
Alpha 1 effects: > 10 mcg/kg/min
Dopaminergic effects: 0.5-2 mcg/kg/min
Inotropes (Beta Selective)
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
Inodilators
-Milrinone
phosphodiesterase type II inhibitor
non catecholamine inodilator
—-increased CO w/ reduction in arterial pressure, LVED, and pulmonary vascular resistance
