Dopamine has unique adverse endocrine effects. Dopamine may directly stimulate diuresis via action on dopamine-receptors, thereby falsely suggesting that renal perfusion is adequate.
There is a relatively high risk of tissue necrosis if it extravasates. Dopamine may cause greater malperfusion of the gut compared to norepinephrine.
Thus, peripheral vasopressors should be started immediately if the blood pressure or perfusion is inadequate. Norepinephrine is safe for short periods of time through a large peripheral vein.
Ongoing peripheral infusion also appears safe, but this should ideally be done within the context of a well-designed protocol involving frequent monitoring of the extremity and preparation for management of extravasation reaction more on this here.
Ongoing infusion should be avoided in deep ultrasound-guided peripheral IVs, where it may be impossible to monitor the tissue surrounding the end of the IV cannula. Phenylephrine and epinephrine have not been reported to cause tissue necrosis.
Peripheral infusion of these agents appears to be generally safe, although this should still ideally be done via a well-functioning cannula proximal to the wrist more on this here.
Vasopressin should arguably be avoided for peripheral administration, because if it extravasates there is no vasodilatory agent which can counteract its action. Clinician-placed midlines are evolving as an alternative to either ultrasound-guided peripheral IVs or central lines. This is a rapidly emerging topic. Overall, vasopressor administration via midline catheters appears to be safe. Some evidence suggests that ongoing midodrine therapy in patients with cirrhosis may support renal perfusion given that these patients suffer from chronic vasodilation.
Dose range is mg q8hr Midodrine is cleared by the kidney, so exercise caution in renal dysfunction. This is a potentially dangerous way to increase blood pressure, because it could potentially impair microvascular perfusion. Historically, a nitric oxide synthesis inhibitor was shown to increase mortality in septic shock This could restore mitochondrial function in some situations where parts of the electron transport chain are dysfunctional, for example metformin toxicity Especially following cardiothoracic surgery.
Possibly also: septic shock, anaphylaxis. If no response, then try another medication or treatment strategy. If response seen, then consider initiating an infusion… 2 Infusion: Dose range from 0.
May be continued for up to hours. Wean off when hemodynamics improve. This may be more of a problem at higher doses. High levels of methylene blue can interfere with pulse oximetry a problem mostly when giving the bolus dose. Selby reports no financial relationships relevant to this field of study. SYNOPSIS : When studying cardiogenic shock after acute myocardial infarction, these investigators found using epinephrine compared to norepinephrine produced similar effects on blood pressure and cardiac index, but resulted in a higher incidence of refractory cardiogenic shock.
Epinephrine versus norepinephrine for cardiogenic shock after acute myocardial infarction. J Am Coll Cardiol ; A mong patients with acute myocardial infarction AMI , the development of cardiogenic shock CS is associated with high mortality.
Vasopressors are used to raise blood pressure and maintain end-organ perfusion, with epinephrine and norepinephrine the two most commonly used agents. However, data directly comparing the effects of epinephrine and norepinephrine in CS are lacking. In a multicenter, prospective, double-blind study, Levy et al randomized 57 patients with CS after AMI to epinephrine vs. In both groups, the study drug was titrated for a target mean arterial pressure MAP of mmHg.
The primary efficacy outcome was the change in cardiac index at 72 hours. A randomized control, double-blind clinical trial suggested that the use of epinephrine approximates the combined use of norepinephrine and dobutamine, but it demonstrated increased lactate levels in the peripheral tissues due to local ischemia Thus, epinephrine is considered as an adjunct agent to norepinephrine if the MAP is not adequately increased.
Vasopressin is an endogenous peptide hormone released by the neurohypophysis promoting non-adrenergic vasoconstriction, especially in sepsis-associated hypotension. In the early phases of shock, the endogenous vasopressin stores become depleted.
Vasopressin is used as a catecholamine-sparing agent to reduce the levels of norepinephrine dosage Inotropic support in septic shock patients is used when there is evidence of myocardial dysfunction as suggested by low CO, increased filling pressures and persistent hypoperfusion despite optimal fluid resuscitation and use of vasopressors.
Besides, the dysregulated cardiac contractility is a mixture of altered cellular metabolism and autoregulatory mechanisms in the microvasculature of the heart per se Dobutamine is the first-line inotropic agent in septic patients as suggested by the SSC. Milrinone is recommended only in patients that are chronically beta-blocked or with chronic heart failure whose adrenergic receptors are desensitized Levosimendan is not currently used in septic shock.
Further investigations may shed light upon the use of agents that increase cytoplasmic calcium. Anaphylaxis is a severe, life-threatening generalized or systemic hypersensitivity reaction that requires immediate and adequate care In recent years, an increase in anaphylaxis incidence rates has occurred and, thus, more light should be shed upon this issue Rapid recognition of anaphylaxis and prompt initiation of treatment is the cornerstone to reduce mortality rates.
The first-line therapy is intramuscular injection of epinephrine, then removal of the allergen and, finally, monitoring of the airway, circulation, breathing and mental status Epinephrine is used as the first step of anaphylaxis treatment owing to its alpha-1 agonist effects that prevents airway edema, hypotension and, eventually, shock along with its beta-2 agonist effects that induces bronchodilation 6.
However, as discussed above, epinephrine administration could have detrimental effects in patients with cardiovascular diseases. Moreover, endogenous and exogenous catecholamines play a significant role in the pathophysiology of Stress-Induced Cardiomyopathy Takotsubo cardiomyopathy.
Although rare, this mandates that epinephrine use should be monitored especially since no guidelines suggest any other therapy as a substitute. The potential long-term adverse effects of epinephrine use in this kind of patients should be balanced with the acute management of the fatal risk of anaphylaxis Besides, clinicians should keep in mind that anaphylaxis itself could affect the myocardium in a condition called the Kounis Syndrome In any case, Guidelines recommend early epinephrine administration in every patient with anaphylaxis with no absolute contraindication in its use.
The only considerations are in the elderly people that are beta-blocked due to the unopposed alpha-1 adrenergic effects and the reflex vagotonic effects. Neurogenic shock is a common cardiovascular dysfunction seen in the acute stage after spinal cord injury, characterized by significant hypotension as well as bradycardia.
The changes in the hemodynamic profile are the result from the loss of supraspinal sympathetic excitatory input to sympathetic pre-ganglionic neurons, which are crucial for maintaining BP The profound hypotension resulting from neurogenic shock leads to microvascular hypoperfusion of the spinal cord.
This vicious cycle of microcirculation affects neurological recovery rates According to the Consortium for Spinal Cord Medicine, injuries at the cervical level and at the thoracic until T6 demand a vasopressor agent with both inotropic and vasoconstrictive properties to support both the vessel tone and cardiac contractility given the fact that sympathetic innervation of the heart originates at the level T1—T4 Thus, dopamine and norepinephrine are the agents used at this specific injury level.
Injuries in lower thoracic and lumbar level warrant the need of a specific peripheral vasoconstrictor such as phenylephrine, which acts only on alpha-1 receptors. Epinephrine is not widely used in neurogenic shock because it exerts its beta-1 adrenergic effects leading to arrhythmias requiring continuous monitoring Dobutamine is not used in neurogenic shock because of its peripheral vasodilatory properties and potential reflex bradycardia The most common inotropic and vasopressor agents used in everyday clinical practice for shocked patients, their receptors, actions and role in therapy are presented in Table 1.
Fluid resuscitation, vasopressors and inotropes are the first line medication for the different types of shock due to their mechanism of action and their well-established clinical outcome 2 , 9.
However, as experimental research and clinical trials are constantly being published, new suggestions appear regarding alterations and novelties in the use of these medications in the management of shock Tables 2 , 3.
For these reasons, there is a trend to use norepinephrine as a safer agent in the case of cardiogenic shock 1 , 2. One more comparison between norepinephrine and dopamine revealed that norepinephrine remains the most appropriate medication and first line drug in cardiogenic shock due to the fact that the dopamine produces more arrhythmic events in patients and carries a higher mortality rate 3 , 4.
Recent data suggest norepinephrine as a more useful drug in cardiogenic shock instead of the broadly used epinephrine and dopamine. Regarding vasopressin, no new recommendations can be made as there are no clinical trials comparing it to norepinephrine 1 , 4 , 5. However, there are some indications suggesting treating patients with vasopressin instead of norepinephrine when the second one produces detrimental tachycardias 6 , 7. Furthermore, there is a limitation in epinephrine administration in hypotensive patients 8.
As far as inotropes are concerned, it is well established that dobutamine is administrated at the same time with norepinephrine in order to maximize the contraction of the heart. On the other hand, no novel data regarding inotropes, such as levosimendan and phosphodiesterase inhibitors, have been published, suggesting no new perspectives in cardiogenic shock, except for some new evidence that failed to report any benefit from levosimendan in organ protection and mortality rate 4 , 8 - The inotropic support in patients with hypotension or vasoplegia must be started after vasopressors such us norepinephrine; however, in case of patients with normal BP, the first step is the use of inotropes dobutamine for cardiogenic shock 6.
One benefit of inopressors over other options is the ability to infuse them through a peripheral intravenous line. Although most of the literature on this topic is derived from case studies 15 , several recent studies demonstrate the safety of the catecholamine-based pressors when given through a peripheral catheter. In a prospective, observational study performed in , patients were given phenylephrine, norepinephrine, or dopamine through a peripheral catheter for an average duration of 49 hours A similar study in corroborated these results Until more rigorous research is performed on the topic, this technique is an acceptable temporizing measure, but central access should be obtained as soon as possible for long-term use we recommend within 4 hours of beginning the inopressor and regular reassessment of the extremity and IV line.
If using peripheral vasopressors, it is important to place the catheter as proximally as possible If extravasation occurs, use phentolamine 0. A year-old male presents to the trauma bay after jumping off a bridge.
His GCS is He is alert but oriented only to person and place. He complains of severe neck pain. On exam, he has obvious deformities that are consistent with closed fractures of his upper and lower extremities.
Upon examination of his spine, you note palpable midline tenderness and step-offs at multiple levels. Norepinephrine primarily stimulates alpha-1 and alpha-2 receptors, acting as a balanced venous and arterial vasoconstrictor. Norepinephrine also results in a small amount of beta-1 agonism, thereby producing a modest inotropic effect. Its effect on the arterial system theoretically leads to increased coronary blood flow and afterload, while its effect on the venous system effectively mobilizes the physiologic venous reserve, offering increased preload Norepinephrine is considered safer than both epinephrine and dopamine.
The same study found norepinephrine superior in improving central venous pressure, urinary output, and arterial lactate levels compared to epinephrine, phenylephrine, and vasopressin. However, norepinephrine was not associated with a mortality benefit or improved hemodynamic endpoints.
In addition, several studies have demonstrated that while norepinephrine increases MAP and cardiac index, it may not improve end-organ flow as measured by splanchnic circulation Although norepinephrine is largely considered to be the safest inopressor, it still carries a risk of toxicity to cardiac myocytes, cardiac arrhythmias, and peripheral vasoconstriction leading to tissue ischemia It is the first-line pressor choice in distributive shock, including both neurogenic 24, 25 and septic shock 4.
Although previous guidelines included epinephrine as an alternative first-line agent for septic shock, the most recent Surviving Sepsis Campaign guidelines, published in , recommend norepinephrine as the only first-line pressor 4. Norepinephrine is considered first-line in cardiogenic shock with profound hypotension systolic blood pressure less than 70 mm Hg 26, It should be used in conjunction with dobutamine in patients with cardiogenic shock and blood pressure higher than 70 mm Hg who fail to respond to dobutamine.
Several intensivists suggest using weight-based dosing to avoid the adverse effects associated with norepinephrine use Norepinephrine has a rapid onset of action, so the effects should be seen within minutes, and the dose can be titrated every minutes.
A year-old female with no past medical history presents to your emergency department with extreme shortness of breath after being stung a bee just prior to arrival. She is in moderate respiratory distress, speaking only in word phrases. On exam, you note moderate stridor, oropharyngeal swelling, diffuse expiratory wheezes, and a diffuse urticarial rash.
You treat her with intramuscular epinephrine, in addition to intravenous steroids, diphenhydramine, 2L LR, and ranitidine. Epinephrine stimulates beta-1 and beta-2 receptors, resulting in substantially more inotropic effects than norepinephrine. Due to its beta-agonism, epinephrine greatly increases heart rate and stroke volume, with a small amount of bronchodilation. Epinephrine also has a moderate stimulatory effect on alpha-1 receptors, leading to modest peripheral vasculature effects.
At lower doses, epinephrine acts primarily as a beta-1 agonist; at higher doses, it acts primarily as an alpha-1 agonist Epinephrine is associated with an increased risk of tachycardia and lactic acidosis Although the exact cause for the lactic acidosis is unknown likely due to enhanced beta agonism triggering lactic acid production and release , no studies demonstrate increased mortality or serious adverse events associated with epinephrine use 28, 29 ; this increase may not be related to tissue hypoperfusion.
Due to its potential for deleterious effects, current Surviving Sepsis Campaign guidelines recommend using epinephrine as a second-line agent, after norepinephrine 4. This can be used with norepinephrine if cardiac contractility is decreased on US.
In , a multinational, prospective randomized control trial RCT of patients with cardiogenic shock found epinephrine to be independently associated with increased day mortality and worsened renal function compared to dobutamine and norepinephrine These results have not yet been validated by further studies.
However, due to these findings, in addition to known increased incidence of arrhythmogenic events associated with epinephrine, it should be used with extreme caution in cases of cardiogenic shock.
Due in part to its stimulatory effect on beta-2 receptors leads to bronchodilation, epinephrine is widely regarded as the first-line agent for anaphylactic shock The current guidelines for anaphylactic shock recommend an initial bolus of 0. However, several studies have demonstrated increased incidence of adverse events associated with intravenous epinephrine.
For the same reasons as those discussed for norepinephrine, weight-based dosing is probably ideal. In the setting of septic shock, start epinephrine at 0. An year-old male with unknown past medical history is brought to your emergency department via EMS.
Family called EMS because the patient is normally ambulatory and active, but has been increasingly somnolent and diffusely weak for the past several days. His initial vital signs reveal a rectal temperature of
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