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New Nurse Podcast

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As a new nurse you might be worried about killing your patient. This podcast will help you avoid doing that by teaching you what to do if you find yourself in a "worst case scenario" in the ICU..

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Recent Episodes

What’s in your IV bag?
Ever wondered what kind of fluids are hanging in your IV bag and why? Hopefully, this audio podcast will answer all of your questions about: Crystalloids Isotonic Solutions: Normal Saline, Lactated Ringers, D5W Hypotonic Solutions: D51/2 NS, .45% NS, D5W Hypertonic Solutions: D5NS, D5LR, 3% NS, 10%NS Colloids Hetastarch, Albumin, Mannitol, Dextran    
Vasoactives and Low Blood Pressure Part II
Dopamine/Inotropin Dopamine is a dose dependent medication, meaning it activates different receptors depending upon the dose given.  Low dose activates dopaminergic receptors which causes vasodilation.  At 2-10 mcg/kg/min, beta 1 is stimulated and you get increased cardiac contractility making this a positive inotrope.  This should be easy to remember since the name of the drug is Inotropin!  At 5-10mcg/kg/min, cardiac output is increased secondary to an increase in stroke volume (SV).  Remember that Cardiac Output (CO)= SV + Heart Rate (HR).  Lastly, a dose 10 mcg/kg/min activates alpha receptors and causes vasoconstriction. Dopamine is used with septic shock and cardiogenic shock. Dobutamine/Dobutrex Dobutamine is a positive inotrope (increases cardiac contractility), a positive chronotrope (increases heart rate) and it causes vasodilation.  The vasodilation decreases systemic vascular resistance (SVR) and increases cardiac output. Dobutamine is used for severe heart failure that is refractory to other medical treatments.  It is also used in cardiogenic shock (e.g. a patient who has had a severe myocardial infarction). Vasopressin Vasopressin is synthetic ADH (anti-diuretic hormone).  In our body, natural ADH helps our bodies conserve water by acting on the kidneys.  In high drip concentrations, Vasopressin causes increased peripheral vascular resistance through arterial vasoconstriction- which hopefully aids in the increase of blood pressure.  This is easy to remember because Vasopressin sounds just like vasopressor. Normally, Vasopressin is ordered at a set rate and is not titrated.  Vasopressin is used in hypovolemic shock and can be ordered alongside other vasoactive medications for hypotension with the goal of reducing pressor demands.  Basically, the goal with hanging Vasopressin is to help wean down other vasoactive drips. Complications There are many complications to using vasoactive medications, which is why they are only used in shock. Hypoperfusion Hypoperfusion can be seen in the extremeties, mesenteric organs, and kidneys.  Check your patient’s fingers and toes for color.  Hypoperfused digits will appear dusky and then necrotic.  They may be cool and will have poor capillary refill.  Assess bowel sounds and monitor strict intake and output. Dysrhythmias Dysrhthmias are often from stimulation of beta 1.  Sinus Tachycardia is the most common, but patients can also convert into Atrial Fibrillation and ventricular tachyarrythmias.  Ensuring that your patient has been adequately fluid resuscitated can help minimize the frequency of dysrhythmias as well as limit the severity of injury from a dysrhythmia.  If you have a patient on a vasoactive medication and you notice that the heart rate is trending higher as you titrate the medication, notify the healthcare provider immediately.  You should also notify the health care provider of any change to heart rhythm and of increased ectopy (PVC’s, PAC’s, etc.) Myocardial Ischemia Vasoactive medications can make the patient’s heart work harder which in turn increases myocardial oxygen consumption.  Luckily, many of the drugs cause dilation of the coronary arteries but sometimes this is not enough.  Look for any ST elevation or ST depression on the cardiac monitor and notify the MD. Extravasation/Necrosis Local vasoconstriction at the IV site is a risk with most vasoactive medications.  If you have to use a peripheral IV, use a large vein, like the antecubital vein.  Check your facility policy, as some medications need to be moved to a new peripheral IV site every 12 hours or so.  Ensure your patient has two good IV sites in case one becomes extravasated.  Better yet, obtain a central line for access from the health care provider. Miscellaneous Drips can be standard concentrated or double concentrated There is no set way to titrate medications, be aware of your minimum and maximum and titrate up or down slowly unless your patient is not responding to small increases- then it may be beneficial to titrate up faster Most of the vasoactive drugs are compatible and can be hung in the same line Label your drips and date your drugs!  Drugs can expire in 12-24 hours Document vital signs every 15 min or 30 min depending on your policy Know how much drug you have left in the drip bag and order a new bag from pharmacy when you hang your last bag Request an arterial line from the healthcare provider to ensure more effective drug titration
Vasoactives and Low Blood Pressure Part I
Definitions Vasoactive is an umbrella term for any drug that makes your heart rate and/or blood pressure go up or down. Vasopressor, on the other hand, is a term for a drug that makes your blood pressure goes up by the process of vasoconstriction (squeeze). A positive inotrope is different from a vasopressor in that an inotrope affects cardiac contractility in a positive way- e.g. it makes your heart pump stronger. So a positive inotrope increases the strength of the muscular contraction and a negative inotrope weakens the strength of the muscular contraction. Some drugs act as both a vasopressor and an inotrope. Drugs can also effect chronotropy which simply means a change in heart rate. Positive chronotropy means an increase in heart rate and negative chronotropy means a decrease in heart rate. You should be slightly familiar with the idea of drug receptors if you want to understand how our ICU vasoactive drugs work. The drugs we give our patients have neurotransmitters that land on receptor sites and act as either agonists or antagonists. Agonists stimulate the response and antagonists block the response. Cholinergic nerves release acetylcholine and are part of the parasympathetic nervous system. The parasympathetic system is our “rest and digest” system. Activation makes blood vessels dilate, heart rate slow, pupils constrict and makes you secrete more saliva. Anticholinergics block vasodilation and decrease saliva secretion. Atropine is a good example of an anticholinergic- it competes for receptor sites to blocks the effect of the parasympathetic nervous system and the vagal nerve. The vagal nerve can be responsible for bradycardia. This is why you sometimes hear a nurse or health care provider say the patient has vagal’d down or brady’d down when the patient drops their heart rate suddenly. Adrenergic nerves release epinephrine, norepinephrine and dopamine and are part of the sympathetic nervous system, our “fight or flight” system. Norepinephrine primarily actives alpha 1 receptors in vascular walls, which causes increased vasoconstriction. Epinephrine primarily activates beta receptors but sometimes activates alpha receptors as well. Beta 1 receptors are most commonly found in your heart and beta 2 receptors are most commonly found in your lungs. An easy way to remember this is to remember that you have 1 heart (beta 1) and you have 2 lungs (beta 2). Activation of beta 1 receptors increases contractility (a positive inotropic effect) and also increases heart rate (a positive chronotropic effect). Beta 2 receptor activation causes bronchodilation in the lungs and causes vasodilation in the vascular smooth muscule. When epinephrine activates alpha receptors, we get local vasoconstriction. Adrenergic blocking agents are in the anti-hypertensive drug category because they block the alpha and beta effects, thereby causing relaxation of smooth muscle and preventing the fight or flight response from taking over. Dopamine receptors are found in renal, mesenteric, coronary, and cerebral vascular beds. When dopamine receptors are stimulated, the result is vasodilation. Side Notes It is important to understand the mechanism of action for the vasoactive drugs we use in the ICU. As we mentioned earlier, some drugs may activate multiple receptors and have varied responses. Also, some drugs activate certain receptors at a lower dose and additional receptors at a higher dose. The prescriber does not randomly choose a vasoactive medication. Careful thought should go into determining why the patient is hypotensive before choosing the best vasoactive medication to reverse the hypotension. Does the patient need an increase in vasoconstriction or an increase in heart muscle strength? Vasoactive medications are dangerous drugs with many side effects and are therefore only used in a monitored unit for patients who are in shock. Neosynephrine/Phenylephrine Neosynephrine may also be referred to as “Neo” in the ICU. It is a pure alpha adrenergic so it causes vasoconstriction. The vasoconstriction increases systemic vascular resistance (SVR), which in turn increases the mean arterial pressure (MAP). If you were giving Neosynephrine to a patient with a pulmonary artery catheter, you should see an increase in your SVR values. An increase in SVR can sometimes mean a decrease in cardiac output because an increase an SVR makes the heart work a little harder to pump blood out against the squeezing/vasoconstricting vessels. Therefore, this drug may not be the best choice for a patient with heart dysfunction. In addition to being a vasoconstrictor, Neosynephrine has some positive inotropic and chronotropic action. This means Neosynephrine may slightly increase cardiac contractility and slightly increase the patient’s heart rate. Norepinephrine/Levophed Norepinephrine may also be referred to as “Norepi” or “Levo.” It is an alpha and beta adrenergic agonist as well as a sympathomimetic drug. Sympathomimetic drugs mimic the sympathetic nervous system, so we get a fight or flight type response. Norepinephrine causes potent vasoconstriction and has a small positive inotrope effect so you may see a small increase in your patient’s cardiac output. In addition, Norepinephrine dilates the coronary arteries to help deliver more oxygen and nutrients to the heart muscle. This is a result of the beta adrenergic agonist response. With Norepinephrine, the MAP is elevated by severe vasoconstriction. Fluid resuscitation is important for patients on pressors so you’ll often given a fluid bolus before starting a pressor and start a maintenance fluid like Normal Saline 0.9% or Lactated Ringers. If the patient is in hemorrhagic shock, where the problem is loss of blood, you should replace blood products and give fluid before hanging a pressor. You can’t squeeze a dry tank! If you squeeze a dry tank, you may see renal failure (decreased urine output), tissue hypoxia/ischemia and lactic acidosis and meanwhile your monitor is telling you the blood pressure is adequate. Why? Because it is measuring the amount of squeeze in the vessels, not delivery of oxygen and nutrients to the tissues. That’s why we look at the entire patient, not just the monitor. Signs of poor cardiac output are dusky skin, cold and clammy skin, and decreased urine output. Norepinephrine also has a small positive chronotropic effect that gets cancelled out by reflex bradycardia (caused by the increase in MAP). As a result, your patient’s heart rate usually stays the same or decreases slightly. Norepinephrine is used as a first line treatment for septic shock. Epinephrine/Adrenalin Epinephrine may also be referred to as “Epi” in the ICU. Epinephrine is a potent beta 1 agonist and a moderate beta 2 (vasodilation) and alpha 1 (vasoconstriction) agonist. The beta 1 agonist effects include increased inotropy and chronotropy and unfortunately the beta 1 activation puts the patient at risk for cardiac dysrhythmias due to the beta 1 stimulation in the heart. So when you’re giving Epinephrine, you may start to see ectopy on the cardiac monitor. We will talk about this more in Part 2 where we go over complications of vasoactive medications. Epinephrine is a dose dependent drug, so at lower doses you see different effects than you would in higher doses. At low doses, there is more vasodilation as a result of beta 2 receptor stimulation in the muscles and the liver. At low to moderate doses, Epinephrine should give your patient an increased cardiac output and a decreased SVR but you may not see much of a change in your MAP. At higher doses of Epinephrine, there is more vasoconstriction secondary to alpha 1 activation. Epinephrine is second line treatment for septic shock and first line treatment for anaphylactic shock. Post operative cardiac surgery patients are usually on Epinephrine drips as well because of the positive inotropy and positive chronotropy. See Part II for information on Dopamine, Dobutamine, Vasopressin, and a discussion of complications and tips for ICU drips.
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Podcast Details
Started
Nov 18th, 2010
Latest Episode
Dec 30th, 2011
Release Period
Monthly
No. of Episodes
17
Avg. Episode Length
31 minutes
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No
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