Tumescent Solution (for burn surgery and liposuction and other things too)

tumescent_a

Tumescent solution is also called “Klein’s Solution” after the physician who characterized the recipe and the use of it.

It’s called “tumescent” because it makes things tumescent, which is a fancy word for swollen. Tumescent is a dilute solution of lidocaine, epinephrine, and sodium bicarbonate that is injected in the subcutaneous tissue (fat). The epinephrine is the most important ingredient as it causes vasoconstriction, this means that the blood loss that could be a big problem for large procedures like burn surgery and liposuction becomes much less of a big deal.

The other interesting thing is that since fat is relatively avascular compared to other tissues, the “safe amount” of tumescent is much higher than what is normally stated for injections of lidocaine or epinephrine.

For example, it was reported by Klein that the toxic dose of lidocaine for tumescent solution is 35 mg/kg of body weight.

There are a few different recipes for tumescent anesthesia, the one presented in the doodle is the one first outlined by Klein, some use more or less lidocaine or epinephrine.

References

  1. Kucera IJ1, Lambert TJ, Klein JA, Watkins RG, Hoover JM, Kaye AD. Liposuction: contemporary issues for the anesthesiologist. J Clin Anesth. 2006, 18(5): 379-87.
  2. Klein JA. The tumescent technique. Anesthesia and modified liposuction technique. Dermatol Clin. 1990, 8(3): 425-37.
  3. Klein JA. Tumescent technique for local anesthesia improves safety in large-volume liposuction. Plast Reconstr Surg. 1993, 92: 1085-100.

Jugular Venous Pulse (JVP)

jvpThe jugular venous pulse/pressure (JVP) is a favourite topic on the wards!

The jugular veins fill with blood and pulsate in relation to filling in the right atrium. Since the JVP correlates well with central venous pressure, it’s used as an indirect marker of intravascular fluid status.

Traditionally, the right internal jugular (IJ) vein is used in JVP measurement; it’s preferred since it is directly in line with the superior vena cava and right atrium. The external jugular (EJ) vein is not commonly used to assess the JVP because it has more valves and an indirect course to the right atrium, but EJ is easier to see than IJ, and JVP measurements from both sites correlate fairly well. The left-sided jugular veins are also uncommonly used, since they can be inadvertently compressed by other structures and thus be less accurate!

Learners on the ward are often asked how to identify the JVP and distinguish it from carotid artery pulsations. The mnemonic POLICE describes the distinguishing features of the JVP:

  • Palpation: The carotid pulse is easy felt but the JVP is not.
  • Occlusion: Gentle pressure applied above the clavicle will dampen the JVP but will not affect the carotid pulse.
  • Location: The IJ lies lateral to the common carotid, starting between the sternal and clavicular heads of the sternocleidomastoid (SCM), goes under the SCM, and when it emerges again can be followed up to the angle of the jaw. The EJ is easier to spot because it crosses SCM superficially.
  • Inspiration: JVP height usually goes down with inspiration (increased venous return) and is at its highest during expiration.
    • (Kussmaul’s Sign describes a paradoxical rise in JVP during inspiration that happens in right-sided heart failure or tamponade)
  • Contour: The JVP has a biphasic waveform, while carotid pulse only beats once.
  • Erection/Position: Sitting up erect will drop the meniscus of the JVP, while lying supine will increase filling of the JVP.

To measure the JVP, the patient lies supine in bed at a 30 – 45 degree angle, with their head turned slightly leftward and jaw relaxed. A hard light source (e.g., penlight) pointed tangential to the patient’s neck will accentuate the visibility of the veins. Once the highest point of JVP pulsation is seen, measure high how it is at its maximum, in terms of centimeters above the sternal angle (aka Angle of Louis, at the 2nd costal cartilage). The JVP normally is 4 cm above the sternal angle or lower; increased in fluid overload and decreased in hypovolemia.

  • Beigel R et al. 2013. Noninvasive evaluation of right atrial pressure. Journal of the American Society of Echocardiography: 26;1033.
  • Chua Chiaco JMS, Parikh NI, Fergusson DJ. 2013. The jugular venous pressure revisited. Cleveland Clinic Journal of Medicine. 80;638.
  • Cook DJ, Simel DL. 1996. Does this patient have abnormal central venous pressure? Journal of the American Medical Association: 275;630.
  • Vinayak AG, Pohlman AS. 2006. Usefulness of the external jugular vein examination in detecting abnormal central venous pressure in critically ill patients. Archives of Internal Medicine: 166;2132.
  • Wang CS et al. 2005. Does this dyspneic patient in the emergency department have congestive heart failure? Journal of the American Medical Association: 294;1944.

Clotting Cascade – NOW WITH NOACs

clotting_cascade_NOAC

The clotting cascade was one of the first doodles posted on Sketchy Medicine, I’ve now updated it to include some of the Novel Oral Anticoagulants (NOACs): Dabigatran, Rivaroxaban and Apixiban.

Dabigatran (Pradaxa)

  • Selective, reversible direct thrombin inhibitor
  • Is actually a prodrug that reaches peak concentration 2-3 h post ingestion
  • Approved (in Canada) for:  Thromboprophylaxis in atrial fib, post-op, and treatment of VTE and VTE recurrence
  • T1/2: 7-17 h
  • CYP independent (not as many drug-drug interactions)
  • Excreted in urine 95% / Feces 5%
  • Reversal: hemodialysis?
  • Big trial = RELY, REMEDY

Rivaroxaban (Xarelto)

  • Selective, reversible direct factor Xa inhibitor
  • Approved (in Canada) for:  Thromboprophylaxis in atrial fib, post-op, and treatment of VTE and VTE recurrence
  • T1/2: 3-9 h (relatively speedy!)
  • CYP3A4
  • Very good oral bioavailability
  • Almost all of it is protein-bound in the serum
  • Urine 70% / Feces 30%
  • Reversal: ???? (not hemodialysis)

Apixaban (Eliquis)

  • Selective, reversible direct factor Xa inhibitor
  • Approved (in Canada) for:  Thromboprophylaxis in atrial fib, post-op, and treatment of VTE and VTE recurrence (only atrial fib in the USA)
  • T1/2: 8-15
  • CYP3A4
  • Almost all (95%) protein-bound in the serum
  • Urine 30% / Feces 70%
  • Reversal: ???? (not hemodialysis)

Reversal agents:

  • Hemodialysis
    • Only good for agents that aren’t highly protein bound (i.e. dabigatran).
    • Warfarin, rivaroxaban and apixaban are all mostly bound to protein in the serum, so dialysis won’t get rid of them
  • PCC
    • Plasma-derived product containing factors II, IX and X (3-factor PCC) or II, VII, IX and X (4-factor PCC) in addition to variable amounts of proteins C and S, and heparin
  • aPCC
    • Plasma-derived product containing activated factors II, VII, IX and X
  • Recombinant factor VIIa
    • Looks good in test tubes, clinical evidence lacking
  • Idarucizumab
    • Humanized monoclonal antibody against dabigatran
  • Andxanet alfa
    • Recombinant factor Xa derivative
    • Could theoretically be used for rivaroxaban and apixaban

Anticoagulation Assays

Effect of oral anticoagulants on coagulation assays (Jackson II & Becker, 2014)

(Adapted from Jackson II & Becker, 2014)

Approach to bleeding

Managing target-specific oral anticoagulant (Siegal, 2015)

(From Siegal, 2015)

References

  • Jackson II LR & Becker RC. (2014). Novel oral anticoagulants: pharmacology, coagulation measures, and considerations for reversal. Journal of Thrombosis and Thrombolysis, 37(3), 380-391.
  • Ufer M. (2010). Comparative efficacy and safety of the novel oral anticoagulants dabigatran, rivaroxaban and apixaban in preclinical and clinical development. Thrombosis and Haemostasis. 103: 572-585.
  • Siegal DM. (2015). Managing target-specific oral anticoagulant associated bleeding including an update on pharmacological reversal agents. Journal of Thrombosis and Thrombolysis, 1-8.

Mechanical Ventilation Basics

ventilator

Volume control (VC) and pressure control (PC) are two common modes of positive pressure mechanical ventilation. In VC, the clinician sets the tidal volume that is given for every breath; pressure is allowed to vary over the course of the breath. In PC, the ventilator is programmed to deliver the same pressure throughout inspiration, so tidal volume is allowed to vary based on the pressure and timing settings, as well as the patient’s own lung compliance.

The timing of ventilation can be set according to a trigger. Continuous mandatory ventilation (CMV) involves setting the respiratory rate and having the ventilator deliver breaths at exactly that rate. This is generally used in paralyzed patients (e.g., general anesthesia), where the patient is not expected to trigger any breaths. In Synchronized Intermittent Mandatory Ventilation (SIMV), mandatory breaths are still given but they are synchronized to the patients’ own respiratory efforts (if present). Also, the patient is allowed to take additional breaths on their own. SIMV is often used to wean patients from the ventilator, by decreasing the rate of mandatory breaths and having patients take more of their breaths spontaneously.

Pressure support (PS) is another mode that is used for weaning. No mandatory breaths are programmed. The patient actively takes their own breaths, and the ventilator simply gives an additional boast of inspiratory pressure to help them out.

Positive End Expiratory Pressure (PEEP) is a setting that is used to prevent alveolar collapse, increase functional residual capacity, and generally improve gas exchange. PEEP involves programming a small amount of additional airway pressure (often ~5-10 cmH2O) to be present at the end of expiration.

  • Nugent K, Nourbaksh E (Eds.). 2011. A bedside guide to mechanical ventilation. Createspace.
  • Owens W. 2012. The ventilator book. First Draught.
  • Kacmarek RM, Hess DR. 2008. Mechanical ventilation for the surgical patient. In: Anesthesiology (Longnecker DE, Brown DL, Newman MF, Zapol WM, Eds.). McGraw Hill, New York.

 

Pierre-Robin Sequence

pierre-robin-sequence

Pierre-Robin Sequence is not a syndrome, it’s a sequence. While it is a collection of features, one happens because of the one that came before.

The features are:

  • Retrognathia/micrognathia (posterior mandible or very small mandible)
  • Glossoptosis (downwards/posterior displacement of the tongue due to the small mandible
  • Airway obstruction (because the tongue is in the way)

Pierre-Robin Sequence is associated with cleft palate (50% of children with the sequence have cleft palate). There are two proposed theories:

  1. The first is that the tongue simply gets in the way of the palate from fusing
  2. The second is that the tongue prevents the newly fused palate from staying fused (this is currently the more popular theory)

PRS, though not a syndrome itself, is associated with multiple syndromes including Stickler Syndrome, velocardiofacial syndrome, fetal alcohol syndrome and Treacher Collins Syndrome.

Complex Regional Pain Syndrome

crps

Hypo/Hyperalgesia:Decreased/increased sensitivity to a usually-painful stimulus (e.g., pinprick).
Hypo/Hyperesthesia: Decreased/increased sensation to a usually-innocuous stimulus (e.g., light touch).
Allodynia: Sensation of pain from a usually-innocuous stimulus (e.g., light touch).

Complex Regional Pain Syndrome (CRPS) refers to a chronic neuropathic pain condition with a broad and varied range of  clinical presentations. CRPS patients experience severe pain out of proportion to their original injury, and this may start at the time of injury or weeks later. The pain is described as deep-seated and burning/aching/shooting. Sesnory changes are common, including hypo/hyperesthesia, hypo/hyperalgesia, and allodynia. For instance, many patients describe not being able to tolerate the sensation of bedsheets on their painful limb.

In the affected area, there is often marked edema, temperature asymmetry (usually cooler), and sweating changes (usually increased). Loss of hair and nail growth is common, and disuse of the limb can result in weakness, muscle atrophy, and contractures.

The diagnosis is made clinically, using the Budapest Criteria. Some pain physicians use a nuclear medicine test, three-phase bone scintigraphy, for CRPS diagnosis but this test is becoming less popular, since it has a low positive predictive value.

Budapest Criteria

  1. Pain, ongoing and disproportionate to any inciting event
  2. Symptoms: at least one symptom in three of the four categories:
    • Sensory: reports of hyperesthesia and/or allodynia
    • Vasomotor: reports of temperature asymmetry and/or skin color changes and/or skin color asymmetr
    • Sudomotor/edema: reports of edema and/or sweating changes and/or sweating asymmetry
    • Motor/trophic: reports of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)
  3. Physical Signs: at least one sign at time of evaluation in two or more categories:
    • Sensory: evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or deep somatic pressure and/or 
joint movement)
    • Vasomotor: evidence of temperature asymmetry and/or skin color changes and/or asymmetry
    • Sudomotor/edema: evidence of edema and/or sweating changes and/or sweating asymmetry
    • Motor/trophic: evidence of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)
  4. No other diagnosis better explains the signs and symptoms

CRPS is classified as Type I when there is no apparent history of nerve damage, and Type II when associated with definite peripheral nerve injury. CRPS most commonly occurs following fractures and immobilization, but can happen even with little to no trauma.The pathophysiology is thought to involve autonomic dysfunction and inflammation, but much is still unknown.

CRPS affects females about 2-4 times more often than males, and onset is usually in middle age (though there are rare pediatric cases reported). It is a progressive disease that can result in spread of pain, sensory disturbances, and physical changes to other limbs.

Treatment for CRPS may involve physiotherapy, complementary medicine (e.g., acupuncture, qi gong) psychological therapies, and a variety of pharmacologic (e.g., NSAIDs, anticonvulsants, antidepressants, opioids, ketamine, bisphosphonates) and interventional procedures (nerve blocks, sympathectomy, neurostimulators). As with all things CRPS, there isn’t great evidence for any particular intervention.

  • Harden RN, Bruehl S, Perez RSGM, Birklein F, Marinus J, Maihofner C, Lubenow T, Buvanendran A, Mackey S, Graciosa J, Mogilevski M, Ramsden C, Chont M, Vatine J-J. Validation of proposed diagnostic criteria (the “Budapest Criteria”) for Complex Regional Pain Syndrome. Pain; 150:268.
  • Hord E-D. Complex regional pain syndrome. In: Massachusetts General Hospital Handbook of Pain Management (Eds: Ballantyne JC, Fields HL). Lippincott Williams & Wilkins.
  • Moon JY, Park SY, Kim YC, Lee SC, Nahm FS, Kim H, Oh SW. 2012. Analysis of  patterns of three-phase bone scintigraphy for patients with complex regional pain syndrome diagnosed using the proposed research criteria (the ‘Budapest Criteria’). British Journal of Anesthesia; 108:655.
  • O’Connell NE, Wand BM, McAuley J, Marston L, Moseley GL. Interventions for treating pain and disability in adults with complex regional pain syndrome – an overview of systematic reviews. Cochrane Database of Systematic Reviews; 4:CD009416.
  • Schwartzman RJ, Erwin KL, Alexander GM. 2009. The natural history of complex regional pain syndrome. Clinical Journal of Pain; 25:273.
  • Smith H, Popp AJ. The patient with chronic pain syndromes. In: A Guide to the Primary Care of Neurological Disorders (Eds: Popp AJ, Deshaies EM). Thieme.
  • Tran DQH, Duong S, Bertini P, Finlayson RJ. Treatment of complex regional pain syndrome: a review of the evidence. Canadian Journal of Anesthesiology; 57:149.

Monitoring Neuromuscular Blockade

nmb

As mentioned in a previous post, neuromuscular blocking drugs are used in anesthesia to ensure paralysis during surgery. The degree of neuromuscular block is assessed using nerve stimulation, where two electrodes impose a pulse of current on a peripheral nerve (e.g., ulnar n., facial n., posterior tibial n.) and induce muscle twitches which can then be monitored through the surgery. There are a few different ways to do nerve stimulation :

Tetany: A sustained stimulation (5 s)
Train-of-four (TOF): Four pulses in rapid succession
Double-burst stimulation (DBS): A series of 3 pulses followed after a pause by 2 or 3 pulses.
Post-tetanic potentiation: When a pulse is sent after a tetanic stimulation, it will bring on a stronger twitch than at first.

With non-depolarizing muscle blockers, there is a fade phenomenon where twitch amplitude decreases from the first stimulation. For instance, in a TOF each twitch is weaker than the last; the last twitch is the first to disappear with non-depolarizing blockade, while the first twitch is the last to disappear. This non-depolarizing fade is also seen in DBS and tetany, though there is still post-tetanic potentiation.

With a depolarizing muscle blockade, no fade will be seen. Instead, all twitches in response to stimulation will be uniformly decreased, and there is no post-tetanic potentiation. This pattern is known as a Phase I block. But, if there is a ton of succinylcholine or the blockade is of a long duration, the pattern of response will look like a non-depolarizing block. This would be a Phase II block.

Recovery of neuromuscular function
Throughout a surgery, the TOF ratio is often mentioned as a means of assessing neuromuscular blockade on an ongoing basis. This means dividing the amplitude of the fourth (and most influenced  by neuromuscular blockers) twitch in a TOF by the amplitude of the first (which is the least affected). In normal people, the 4:1 amplitude is the same, for a TOF ratio of 1. In a Phase I depolarizing block, the TOF ratio is also 1. The TOF ratio will be less than 1 in a non-depolarizing block (remember the fade?). It is commonly mentioned that a TOF ratio of 0.7 represents an full recovery of neuromuscular function, but these days it is thought that a TOF ratio of at least 0.9 is needed before extubation.

It is very hard to tell what the TOF ratio is by sight or feel alone! DBS ratio is more sensitive than TOF ratio for assessing neuromuscular block, and it’s easier to gauge by tactile evaluation than the TOF ratio. So, quantitative monitoring by electomyography (EMG), mechanomyography (MMG), or accelerometry is ideal!

  • Fuchs-Buder T. 2010. Neuromuscular monitoring in clinical practice and research. Springer.
  • McGrath CD, Hunter JM. 2006. Monitoring of neuromuscular block. Continuing Education in Anesthesia, Critical Care & Pain; 6:7.
  • Neuromuscular blocking agents. 2006. In: Clinical Anesthesiology (Eds: Morgan GE, Mikhail MS, Murray MJ). Lange.
  • Viby-Mogensen J. 2005. Neuromuscular monitoring. In: Miller’s Anesthesia (Eds: Miller RD, Erikkson LI, Fleisher LA, Wiener-Kronish JP, Young WL). Elsevier.

BOOTS: Predictors of Difficult Bag Mask Ventilation

boots

Bag mask ventilation (BMV) is an important means of ventilating and oxygenating a patient unable to protect their airway, or in respiratory depression. BMV can be useful as a primary airway management modality in a prehospital setting, and it is also a useful rescue maneuver for cases of  difficult endotracheal intubation.

The following patient features, however, will make BMV difficult; this can be remembered with the helpful mnemonic BOOTS:

  • Beard
  • Obese
  • Old Age
  • Toothless
  • Snores

Essentially, BMV can be complicated any condition that impairs formation of an effective mask seal.  Beards can make establishing an adequate seal difficult, as can any disruption of normal facial anatomy (no teeth, facial fractures, excess facial tissue). Individuals aged over 55 years old are considered to be higher risk for BMV, in part because of decreased upper airway muscle tone. Patients should be screened for obstructive sleep apnea before an elective surgery; also, note that conditions increasing airway resistance (e.g., severe asthma) or decreasing pulmonary compliance (e.g., pulmonary edema) can make ventilation challenging.

  • Hung O and Murphy MF (Eds). 2008. Management of the difficult and failed airway. McGraw-Hill.
  • Kovacs G and Law JA (Eds). 2011. Airway management in emergencies. People’s Medical Publishing House-USA.

Induction Agents in Anesthesia

General anesthesia has a bunch of different steps:

  1. Pre-oxygenation/Pre-induction (some people don’t count this as a step)
  2. Induction (putting them “to sleep”)
  3. Maintenance (keeping them asleep)
  4. Emergence (waking them up)

In North America, many physicians like to use a combination of an analgesic and a sedative followed by the induction agent propofol. Sometimes other agents are used for induction such as etomidate or ketamine, particularly if there is a worry about hemodynamic instability as propofol not uncommonly can cause bradycardia and/or hypotension.

If the patient is going to be intubated, a paralytic (muscle relaxant) is also used to relax the vocal cords to prevent unnecessary trauma as the tube is passed through them. Competitive acetyl choline (ACh) receptor antagonists such as rocuronium or succinylcholine are used for this. The main difference between the two is that succinylcholine is a depolarizing agent – meaning that when it first binds to the ACh receptor, it causes a contraction, whereas rocuronium is non-depolarizing – so when it binds nothing happens. So with this pesky contraction thing why would any one choose succinylcholine? The nice thing is that the half-life is much much shorter than rocuronium, so if things don’t work out quite the way you want them to, or you just want something fast, you don’t need to continue to help the patient breath.

Shock

BUY THIS AS A STUDY CARD

Shock is “a syndrome resulting from failure of the cardiovascular system to maintain adequate tissue perfusion.”

Weil-Shubin Classification of Shock

  1. Cardiogenic –  Poor cardiac function reduces forward blood flow.
  2. Hypovolemic – Loss of intravascular volume caused by: hemorrhage, dehydration, third space loss, vomiting, diarrhea.
  3. Obstructive – Impair cardiac filling due to external restriction. Caused by cardiac tamponade, tension pneumothorax, pulmonary embolus.
  4. Distributive – Primarily characterized by loss of peripheral vascular tone. Caused by septic, anaphylactic, adrenal insufficiency, neurogenic, liver failure.

Adrenergic Receptors

  • α1: Vasoconstriction
  • α2: Inhibits norepinephrine release, decreases BP, sedative effects
  • β1: Positive inoptrope (increases cardiac contractility and stroke volume)
  • β2: Vasodilation, broncodilation

Vasoactive Drugs

Epinephrine

  • Effects: Causes vasoconstriction and increases cardiac output. Inotrope effect predominates at low doses (< 4.0 mcg/min).
  • Disadvantages: Associated with lactic acidosis, hyperglycemia, pulmonary hypertension, tachyarrythmias, and compromised hepatosplanchnic perfusion.
  • Use: First-line agent for cardiac arrest and anaphylaxis. Second-line agent for vasopressor and inotrope effects, when other agents have failed.

Norepinephrine

  • Effects: Potent vasoconstrictor. Causes a minor increase in stroke volume and cardiac output.
  • Disadvantages: May decrease renal blood flow and increase myocardial oxygen demand. Extravasation at site of intravenous administration may lead to tissue necrosis.
  • Use: First line therapy for maintenance of blood pressure.

Ephedrine

  • Effects: Increases heart rate, cardiac output. Bronchodilator. Some anti-emetic effects. Longer duration than epinephrine. Has indirect actions on adrenergic system.
  • Disadvantages: Epedrine losses effect with subsequent doses since part of its effect is indirect, by icreasing NE release, which becomes depleted
  • Use: Common vasopressor during anesthesia, but only a temporizing agent in acute shock.

Dopamine

  • Effects are dose-dependent:
    • < 5 mcg/kg/min – Acts at dopamine receptors only, with mild inotrope effect. Vasodilatory effects purported to improve perfusion through renal and mesenteric vessels; however, there is no clear clinical benefit of dopamine on organ function.
    • 5-10 mcg/kg/min – Predominantly β1 adrenergic effects. Increases cardiac contractility and heart rate.
    • >10 mcg/kg/min – Predominately α1 effects, causing arterial vasoconstriction and increased blood pressure. Overall decrease in renal and splanchnic blood flow at this dose.
  • Disadvantages: Has a high propensity for tachycardia and dysrythmias. Potential for prolactin suppression and immunosuppression.
  • Use: First line vasopressor for shock, but may be associated with more adverse outcomes than norepinephrine.

Dobutamine

  • Effects: Racemic mixture. where the L-isomer acts at α1/β1 receptors and D-isomer acts at β1/β2 receptors. Increases cardiac output and decreases systemic/pulmonary cascular resistance. Can increase splanchnic blood flow and decrease endogenous glucose production.
  • Disadvantages: May cause mismatch in myocardial oxygen delivery and requirement. Vasodilation undesirable in septic patients.
  • Use: A ‘gold standard‘ inotropic agent in cardiogenic shock with low output and increased afterload. In sepsis, vasodilatory effects should be counteracted by co-administration with norepinephrine.

Dopexamine

  • Effects: Acts at β2 and dopamine receptors. Causes vasodilation and decreased afterload. Has some positive inotrope effect. Bronchodilatory. Unlike dopamine, dopexamine is not associated with pituitary suppression.
  • Disadvantages: Not widely accepted in practice.
  • Use: Like dobutamine, useful for cardiogenic shock with decreased output and high afterload.

Phenylephrine

  • Effects: Classic selective α1 agonist, causing vasoconstriction. Rapid onset and short duration.
  • Disadvantages: Can reduce hepatosplanchnic perfusion. May cause significant reflex bradycardia.
  • Use: Generally considered a temporary vasopressor until more definitive therapy is begun. Useful for vasdilated patients with adequate cardiac output, for whom other vasopressors present risk of tachyarrhythmias.

Dexmedetomidine/Clonidine

  • Effects: Arousable sedation with preserved respiratory drive. Improved tissue perfusion and renal function. General sympathetic inhibition.
  • Disadvantages: Bradycardia and hypotension.
  • Use: Not used in acute shock setting, but may be useful in later critical care setting.

Vasopressin (not actually an adrenergic drug)

  • Effects: Acts on V1 receptors to cause vasoconstriction. Increases vasculature response to catecholamines.
  • Disadvantages: May cause tachycardia and tachyarrythmias. Excessive vasoconstriction can impair oxygen delivery and and cause limb ischemia.
  • Use: May be used to augment norepinephrine or other agents. Not typically used alone.
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