Swans and Pressors - Vanderbilt University Medical Center...Norepinephrine (Levophed) Stimulates...
Transcript of Swans and Pressors - Vanderbilt University Medical Center...Norepinephrine (Levophed) Stimulates...
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Swans and Pressors
Vanderbilt Surgery Summer School
Ricky Shinall
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Shock, Swans, Pressors in 15 minutes
4 Reasons for Shock 4 Swan numbers to know 7 Pressors =15 things to know
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4 Reasons for Shock
Not enough preload Not enough afterload Not enough contractility Cardiac obstruction
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4 Reasons for Shock
Not enough preload (Hypovol., Hemor.) Not enough afterload Not enough contractility Cardiac obstruction
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4 Reasons for Shock
Not enough preload (Hypovol., Hemor.) Not enough afterload (Neurogenic, Septic) Not enough contractility Cardiac obstruction
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4 Reasons for Shock
Not enough preload (Hypovol., Hemor.) Not enough afterload (Neurogenic, Septic) Not enough contractility (Cardiogenic) Cardiac obstruction
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4 Reasons for Shock
Not enough preload (Hypovol., Hemor.) Not enough afterload (Neurogenic, Septic) Not enough contractility (Cardiogenic) Cardiac obstruction (Obstructive)
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4 Swan Numbers to Know
SvO2 EDVI CI SVR/SVRI
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SvO2: Overall Picture
Normal 60-80%
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SvO2: Overall Picture
Normal 60-80% SvO2=O2 delivery - O2 consumption
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SvO2: Overall Picture
Normal 60-80% SvO2=O2 delivery - O2 consumption SvO2=O2 content x CO – consumption
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SvO2: Overall Picture
Normal 60-80% SvO2=O2 delivery - O2 consumption SvO2=O2 content x CO – consumption SvO2=SaO2 x Hct x CO - consumption
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EDVI: Preload
Normal 100-120
Requires a special type of Swan.
Can also use CVP, PCWP to gauge preload
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CI: Contractility
Normal 2.5-4.0
If your preload and afterload are fixed, CI gives an idea of contractility
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SVR/SVRI: afterload
SVR Normal: 800-1200 SVRI Normal: 2000-2400
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4 Reasons for Shock
Not enough preload Not enough afterload Not enough contractility Cardiac obstruction
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4 Treatments for Shock
Not enough preload – give volume Not enough afterload – squeeze vessels Not enough contractility – squeeze heart Cardiac obstruction – relieve obstruction
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4 Treatments for Shock
Not enough preload – give volume Not enough afterload – squeeze vessels Not enough contractility – squeeze heart Cardiac obstruction – relieve obstruction
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Squeeze Vessels
No heart squeeze Some heart squeeze
Phenylepherine=Neosynepherine Norepinepherine=Levophed
Vasopressin=Pitissin Dopamine
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Squeeze Vessels
No heart squeeze Some heart squeeze
Phenylepherine=Neosynepherine
Norepinepherine=Levophed 1st agent for Sepsis
Vasopressin=Pitissin
Dopamine
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Squeeze Vessels
No heart squeeze Some heart squeeze
Phenylepherine=Neosynepherine
Norepinepherine=Levophed 1st agent for Sepsis
Vasopressin=Pitissin
Dopamine Alternate 1st agent for Sepsis
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Squeeze Vessels
No heart squeeze Some heart squeeze
Phenylepherine=Neosynepherine Neurogenic Shock/Epidural
Norepinepherine=Levophed 1st agent for Sepsis
Vasopressin=Pitissin
Dopamine 1st agent for Sepsis
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Squeeze Vessels
No heart squeeze Some heart squeeze
Phenylepherine=Neosynepherine Neurogenic Shock/Epidural
Norepinepherine=Levophed 1st agent for Sepsis
Vasopressin=Pitissin 2nd agent for Sepsis
Dopamine 1st agent for Sepsis
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Squeeze Heart
Unsqueeze Vessels No Vessel Squeeze
Milrinone Dobutamine
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Epinepherine
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Take Home Points SvO2, EDVI, CI, SVR tell you 95% of the
important info on a Swan Make sure volume status is adequate
before starting pressors Phenylepherine for sympathectomy only Dopamine or Levo for Sepsis, then add
Vaso Dobutamine or Milrinone for contractility Epinepherine if all else fails
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In Depth Info
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Definition of shock
Reduction of systemic tissue perfusion, resulting in decreased oxygen delivery to the tissues.
Prolonged oxygen deprivation leads to cellular hypoxia
The effects of oxygen deprivation are initially reversible, but rapidly become irreversible. The result is sequential cell death, end-organ damage, multi-system organ failure, and death.
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Types of shock
Hypovolemic/Hemorrhagic -loss of blood or plasma volume Cardiogenic
-pump failure or compression Septic
-toxin induced vasodilation Neurogenic - cervical or high thoracic (T1-T5) injury
interrupts thoracic sympathetic outflow
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Physiologic parameters in shock Type of shock CVP/
PCWP CO SVR Venous O2
Sat Hypovolemic (including hemorrhagic)
Cardiogenic
Septic (hyperdynamic)
Septic (hypodynamic)
Neurogenic
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Receptor physiology Alpha adrenergic — Activation of alpha-1 adrenergic
receptors, located in vascular walls, induces significant vasoconstriction.
Beta adrenergic — Beta-1 adrenergic receptors are most common in the heart, and mediate increases in inotropy and chronotropy with minimal vasoconstriction. Stimulation of beta-2 adrenergic receptors in blood vessels induces vasodilation.
Dopamine — Dopamine receptors are present in the renal, splanchnic (mesenteric), coronary, and cerebral vascular beds; stimulation of these receptors leads to vasodilation. A second subtype of dopamine receptors causes vasoconstriction by inducing norepinephrine release.
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Norepinephrine (Levophed)
Stimulates beta1 and alpha-adrenergic receptors.
Clinically alpha effects (vasoconstriction) >> than beta effects (inotropic and chronotropic effects)
Dose 1-30 mcg/min as a continuous infusion Used for treatment of shock which persists after
adequate fluid resuscitation (think sepsis) Adverse reactions: bradycardia, digital ischemia,
skin necrosis (with extrav) Give centrally
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Vasopressin (Pitressin) ADH analog, increases cAMP, direct
vasoconstrictor w/o inotropic/chronotropic effects
Dose 0.01-0.04 units/minute. (Doses >0.04 with more dysrhythmias)
Most case reports have used 0.04 units/minute continuous infusion as a fixed dose for the treatment of septic shock.
Relative deficiency of plasma levels of ADH and relative hypersensitivity to its vasoconstrictive effects during sepsis.
Causes mesenteric vasoconstriction, particularly at higher doses. Also skin necrosis.
Mutlu GM; Role of vasopressin in the management of septic shock. Intensive Care Med 2004 Jul;30(7):1276-91. 2004 Apr 21
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Phenylephrine (Neosynephrine) Alpha-adrenergic stimulator with weak beta-adrenergic
activity Produces systemic arterial vasoconstriction Initial dose: 100-180 mcg/minute, or alternatively, 0.5
mcg/kg/minute; titrate to desired response. Uses: neurogenic shock, hypotension after epidural
placement. Adverse effect: increases afterload and decreases stroke
volume
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Dopamine Adrenergic and dopaminergic agonist Low-dose (dopaminergic): 1-5 mcg/kg/minute, increased renal
blood flow and urine output, mesenteric dilation. Intermediate-dose (dopaminergic and beta1): 5-15
mcg/kg/minute, increased renal blood flow, heart rate, cardiac contractility, and cardiac output
High-dose (alpha-adrenergic predominates): >15 mcg/kg/minute vasoconstriction, increased blood pressure
Good for sepsis or cardiogenic shock Can use on 9N or 10S! Renal Tx service uses
this for hypotension. If extravasates, short half life (2 minutes)
means you can just withdraw the drug. Less likely to cause skin necrosis.
Lauschke A; Teichgraber UK; Frei U; Eckardt KU, “Low-dose' dopamine worsens renal perfusion in patients with acute renal failure.” Kidney Int. 2006 May;69(9):1669-74.
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Epinephrine
Alpha/beta agonist Usually used for shock resistant to other
pressors (or in CT surgery at VA) Causes vasoconstriction, inotropy,
chronotropy Dose: Initial: 1 mcg/minute; titrate to
desired response; usual range: 2-10 mcg/minute
Give centrally
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Inotropes Milrinone
A selective phosphodiesterase inhibitor in cardiac and vascular tissue, resulting in vasodilation and inotropic effects with little chronotropic activity
Dose: 0.375-0.75 mcg/kg/minute. >10%: Cardiovascular: Ventricular arrhythmia (ectopy 9%,
NSVT 3%, sustained ventricular tachycardia 1%, ventricular fibrillation <1%)
Hypotension
Dobutamine Stimulates beta1-adrenergic receptors, causing increased
contractility and heart rate, with little effect on beta2- or alpha-receptors
Dose: 2.5-20 mcg/kg/minute; maximum: 40 mcg/kg/minute, Less arythmogenic than milrinone, but still a concern Hypotension
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Appropriate monitoring
Central line: monitor CVP and for access Arterial line: titrate gtts Foley: monitor end organ perfusion by
following UOP Swan- ganz catheter: optional
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How it works (generally) Measures pressures from the right atrium, right ventricle, and
pulmonary artery. The left atrial pressure can be indirectly measured by inflating a
balloon at the tip of the catheter and allowing the balloon to occlude a branch of the pulmonary artery (PCWP).
The systemic vascular resistance and pulmonary vascular resistance can be estimated by calculations are derived from Ohm's Law
Older pulmonary artery catheters measured cardiac output via the indicator thermodilution method or the Fick calculation.
Newer catheter designs incorporate continuous oximetric monitoring of pulmonary artery oxygen saturation using fiberoptic reflectance spectrophotometry, thereby enabling continuous estimation of cardiac output.
http://www.pacep.org/
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Normal Hemodynamic Parameters
CVP: 1-11 mmHg PCWP: 6-15 mmHg Cardiac output: 4–8 L/min Cardiac index: 2.6–4.2 (L/min)/m2 Stroke volume: 50–100 mL/beat Systemic vascular resistance: 700–1600
dynes · s/cm5 Pulmonary vascular resistance: 20–130
dynes · s/cm5 SVO2: 60-80% (about 75%)