Sedative Medications for Intubated Patients in the ICU

When I first started working in the ICU, I was thrilled by the fact that ICU nurses have a very high level of autonomy when it comes to titrating drugs to keep the patients safe. High autonomy comes with high responsibility that we need to know out drugs well. Today, I would like to discuss about some of the sedative medications for intubated patients. The most common drugs are propofol (Diprivan) and dexmedetomidine (Precedex). Beside my bedside experience from handling these medications, I have used the AACN Essential of Critical Care Nursing by Suzanne M. Burns as my reference to make sure the information is correctly presented. So, let’s learning about some common sedative medications in the ICU and start saving lives!

Before we move on each specific medication, there are some general rules you should be aware.

  • Patient still have pain even when they are appropriately sedated. ICU patients usually have tubes (endotracheal tube, NG tube, G tube, chest tube, Foley, etc) and lines (central line, dialysis, etc) so it is safe to say that almost all of them will experience some kind of discomfort and pain.
  • Sedation can help the patient relax to prevent them from harming themselves from pulling tubes and lines. Sedation also keeps the patients who are on mechanical ventilators from fight the vent.
  • Over-sedation in patients with mechanically ventilator will prolong the weaning process thus keep them on the ventilator longer. Also over-sedation will cause respiratory depression, decreased heart rate and blood pressure.

Propofol (Diprivan)

  • Propofol is a central nervous system depressant. It has a rapid onset and short half life. It is one of the most common sedative medications for patients who is intubated and on the vent. The endotracheal (ET) tube constantly triggers the patients gag reflex which causes extreme discomfort. Therefore, most intubated patients need some sort of sedation to keep them calm and relax.
  • Propofol also decrease cerebral oxygen consumption thus used in patients with traumatic head injury (increased ICP) or status epilepticus
  • Main side effects of propofol include bradycardia and hypotension. Therefore, patients who is on propofol needs to have their vital signs taken every 15 minutes (mainly HR and BP)
  • To appropriately sedate the patient to prevent under-sedation or over-sedation, we use Richmond Agitation Sedation Score (RASS) score to monitor the patient sedation level. We monitor the RASS score every 1 hour in my facility.


The Richmond Agitation and Sedation (RASS) Scale [Digital image]. (2015, March 23). Retrieved April 10, 2018, from

It depends on how much the physician want the patients to be sedated, we usually titrate the propofol to the RASS -2 (patient appears to be asleep, opens eyes for less than ten seconds  and looks at you when you shout his/her name then go back to sleep when is not stimulated. Patient is comfortable, normal heart rate, blood pressure, and not fighting the vent).

  • Dosage 5-100 mcg/kg/min
  • Propofol is formulated in fat-emulsion vehicle which increases growth of microorganism. Therefore, the medication and iv tubing needs to be changed every six to twelve hour (it is every twelve hours in my facility so I usually go ahead and change the whole tubing when I change the first new bag of my shift)
  • High infusion rates (doses greater than 75mcg/kg/min over 48 hours) can cause a rear but serious adverse effect known as propofol infusion syndrome (PRIS). Signs and symptoms of PRIS include hyperkalemia, tachyarrythmia ST-segment elevation in the right precordial leads (V1-V3), bradycardia, rhabdomyolysis, and lactic acidosis (Burns, p.188).
  • Propofol can turn your patient’s urine to green, especially if your patient has been on propofol continuous infusion for several days. This is a harmless side effect which doesn’t require any interventions.

Dexmedetomidine (Precedex)

My facility does not use this drug. Therefore, all information provided here came from the AACN Essential of Critical Care Nursing by Suzanne M. Burns. The reason why I decided to share with you because I learned that Precedex has become quite popular nowadays because it does not cause respiratory depression as much as propofol does thus patient is more awake and ready for weaning trial thus more cases of successful extubation.

  • It is a Alpha 2 adrenergic agonist
  • Used for short term sedation (<24 hours)
  • Decreases HR and BP but does not cause respiratory depression
  • Dose 0.2 to 1.5 mcg/kg/hr

(Burns, p. 188)

Burns, S. M. (2014). AACN essentials of critical care nursing. New York: McGraw-Hill Education.

Learning ABGs as simple as learning ABC’s

img_0153In nursing school, we learned how to correctly interpret ABGs. But, have you ever taken a step further to wonder why it is so important? What does it mean? What type of diseases which reflect that ABGs? What is an “okay” ABG? What is a “very bad” ABG that require immediate intervention? What kind of treatment do we do to bring the patient’s ABG back to normal? In this article, we will have a chance to review how to interpret ABGs as well as answering all these questions. We also will review some case studies which I hope will solidify what you already know about ABGs. So, let’s learn about ABGs and start saving lives.

Before we move on to how to interpret an ABG, let’s review some basic stuff about ABGs. There are four components in the ABGs:

  • pH – A normal pH is 7.35 to 7.45. If your patient’s pH <7.35, your patient is acidotic. If your patient’s pH>7.45, your patient is alkalotic
  • CO2 –A normal CO2 is 3545. If your patient’s CO2 <35, it’s alkalosis. If your patient’s CO2>45, it’s acidosis. Remember, CO2 makes your patient become more acidotic. The more CO2, the more acidosis.
  • HCO3 (bicarb) – A normal bicarb is 22-26. If your patient’s bicarb <22, it is acidosis. If your patient’s bicarb >26, it is alkalosis. Remember, HCO3 (bicarb) makes your patient become more alkalotic. The more bicarb, the more alkalosis
  • pO2 (partial pressure of Oxygen) – A normal is 80%. If your patient’s pO2 is less than 80%, your patient is hypoxic. If your patient’s pO2 is greater than 100%, your patient may receive too much oxygen. Therefore, pay attention to the FiO2 (Fraction of inspire Oxygen). Let’s say if your patient has pO2 of 150% on a vent with FiO2 of 100%, its time to decrease FiO2.

Now that we already familiar with the ABGs value. Let’s interpret an ABG.

There are several steps you should follow so that you can always get it right. Here is an example of an ABG

pH -7.18

pCO2 – 65

HCO3 – 35

pO2  – 45

Whenever I interpret an ABG, I always make a table like this below. I find it easier that way

pH-7.18 CO2 – 65 HCO3 – 35 pO2 – 45


  • Step 1: Before you start to interpret anything, look at the first three values of the ABG. If they are all normal, you have a normal ABG. If not, move on to the second step
  • Step 2: Looking at the pH. Although a normal pH is 7.35 to 7.45, you want to compare your pH value with 7.40
  • If your patient’s pH >7.40, its alkalosis (Yes, I said it 7.40 not 7.45. Therefore, if it’s 7.42, its alkalosis. In that scenario, because it is within normal range of 7.35-7.45, write down “full” for fully compensated. If not, just write down alkalosis).
  • If your patient’s pH <7.40, its acidosis. And again, if pH is within 7.35-7.45, write down “full” for fully compensated. If not, just write acidosis.
pH-7.18 CO2 – 65 HCO3 – 35 pO2 – 45
Since the pH < 7.40



  • Step 3: Looking at the CO2.
  • If CO2 >45, it is acidosis
  • If CO2<35, it is alkalosis
  • If CO2 is within 35-45, it is a normal limit, write uncompensated
pH-7.18 CO2 – 65 HCO3 – 35 pO2 – 45
Since the pH < 7.40


Since the CO2 >45



  • Step 4: Looking at HCO3.
  • If HCO3 >26, it is alkalosis
  • If HCO3 <22, it is acidosis
  • If HCO3 is within 22-26, it is a normal limit, write uncompensated
pH-7.18 CO2 – 65 HCO3 – 35 pO2 – 45
Since the pH < 7.40


Since the CO2 >45


Since HCO3 >26



  • Step 5: As you can see, both pH and CO2 have acidosis, your patient has Respiratory Acidosis. In addition, because the HCO3 is not within normal limit, we see a compensation which the kidney tries to bring the pH back to normal that has not been achieved. So your patient has Partially compensated Respiratory Acidosis.

With the same token, let’s say that your patient has the same pH, same CO2, but HCO3 is 24 which is within normal limit. What do you think your patient have? Yes, it is Uncompensated Respiratory Acidosis which means that even though your patient is in respiratory failure, his/her kidney did not increase HCO3 (bicarb) to bring the pH back to normal.


Here are some more examples you can practice on

Ex 1

pH-7.32 CO2-39 HCO3 -17 pO2-60

Ex 2

pH-7.24 CO2-74 HCO3 -33 pO2-17


Ex 3

pH-7.43 CO2-20 HCO3 -16 pO2-45


Answer Keys

Ex 1

pH-7.31 CO2-39 HCO3 -17 pO2-60
Acidosis Uncompensated Acidosis

-Uncompensated Metabolic Acidosis


Ex 2

pH-7.24 CO2-74 HCO3 -33 pO2-17
Acidosis Acidosis Alkalosis

-Partially Compensated Respiratory Acidosis


Ex 3

pH-7.43 CO2-20 HCO3 -16 pO2-45
Alkalosis and Full Alkalosis Acidosis

-Fully Compensated Respiratory Alkalosis


Now that you have mastered ABGs, Let’s move on to more in-depth topic, the pathology and modalities for each condition. So far we have Respiratory Acidosis, Respiratory Alkalosis, Metabolic Acidosis, and Metabolic Alkalosis.


I find it is very difficult to have a good understanding of those conditions by just memorize the diseases with each condition. So I have created some case study scenario, although I have changed much of the story details to keep patients’ confidentiality to comply with HIPPA regulation, these case studies could be very much true.

  • Let’s imagine. You have a patient who has hx of smoking and diagnosed with COPD several years ago. The patient was admitted to your unit because of shortness of breath, his O2 Sat was 84% on room air. The doctor ordered a Stat ABGs. What do you think his ABGs will look like?


Your patient has hx of COPD, in respiratory distress, bad O2 Sat, what do you think the problem come from? Is it respiratory or metabolic? If it is respiratory origin, is the CO2 going to be high or low? Think about that, if your patient can not breathe, there is probably a decrease in gas exchange resulting in an increased CO2 in the body. So, your patient probably has high CO2 and thus respiratory acidosis. Noted that your patient is breathing fast because he is trying to get some air for gas exchange, what do you think his pO2 going to be? Probably low, right?


  • That is totally different than having a patient who has normal pulmonary and kidney function, coming to the hospital because he failed and fractured his wrist. This patient may have a fast breathing too, but it is because he has pain. So his ABGs probably normal or Respiratory Alkalosis because he blew off too much CO2. This patient will have a low CO2 and normal or high pO2 (which is different than the guy with COPD). The doctor probably does not even bother to get the ABGs because it just a waste of time and resource. What he needs is an X ray and some pain medications. Patients with pneumothorax or pulmonary embolism usually show respiratory alkalosis on ABGs because they hyperventilate.


  • Let’s have another scenario. You have a patient admitted to the hospital because his daughter found him laid unresponsive in the bathroom. He is very altered. Blood test shows that he has a BUN of 110 and Creatinine of 5.5. His total CK is 1,700. His glucose is 900. He is currently breathing fast, respiratory rate of 32, and his O2Sat is 96% on room air. What do you think his ABGs going to look like?

Well, he has some kidney damage probably acute tubular necrosis (ATN) which evident by elevated BUN and Creatinine. Because his kidney is already damage, do you think his bicarb going to high or low? Remember, kidneys conserve and produce bicarb. If the kidney does not work, his bicarb is probably low. What is the condition that involves the kidney and low bicarb? Metabolic Acidosis, right? So, why does the patient is still breathing very fast when we say that he does not have any pulmonary issue? Remember, both lungs and kidneys are working together to compensate to the imbalance to neutralize the pH. If the patient has metabolic acidosis, the lungs will try to get rid of the acidosis part, right? How do the lungs decrease the acidosis? Probably by getting rid of CO2 because it makes the body acidic, right? So that’s why the patient is breathing fast. Also, noted that the patient has a blood sugar of 900, he is probably having a DKA on top of what is going on. Look at his total CK also. It is very high, greater than 1000. He probably has rhambdomyolysis which resulting in release of myoglobin into the blood stream. The myoglobin is a large protein which could cause an obstruction in the nephrons of the kidneys resulting in kidney failure.


  • Another case study? Yeah? You have a patient who has hx of CHF, the patient was admitted to the hospital because of shortness of breath. Blood test showed his BNP was 2,000 and he seemed edematous. So the doctor prescribed Lasix 40mg every 4 hours and 1500mL fluid restriction. Three days later, you the nurse who is assigned to the patient. Upon assessment, you noted that the patient edema had completely gone. The patient became pretty skinny, poor skin turgor. What do you think his ABGs will look like? The patient will have Metabolic Alkalosis. Due to overuse of diuretic, your patient is probably dehydrated. As a result, the kidney increases the HCO3 reabsorption that causes increased bicarb. In general, any volume depletion (including vomiting and diarrhea) could cause Metabolic Alkalosis.

So far we have reviewed how to interpret ABGs and the kinds of disease which reflect each condition. Let’s move on to the next several questions:

What is an “okay” ABG?  What is a “very bad” ABG that require immediate intervention?  What kind of treatment do we do to bring the patient’s ABG back to normal?


  • When we try to figure if an ABG is “okay” or “very bad”, we should think ABCs. Technically, if you have a patient with respiratory problem, you need to be more aggressive to treat the patient. Pt with metabolic problem requires appropriate treatments too, yet it is not as urgent as respiratory issue. In general, patient with respiratory acidosis requires our immediate attention because if your patient is in respiratory distress, he/she could get to respiratory failure at any moment, so the sooner you treat the patient, the better outcome.


  • Treatment usually goes as order, or the physician could jump right into intubation if the ABG result looks bad enough (how bad is bad enough, it’s up to the physician who decides the course of treatment based on the patient’s condition)
    • nasal cannula (1L-6L of oxygen with FiO2 of 24%-44%)
    • then venture mask (which FiO2 could get as high as 50%)
    • then non-rebreather ( which FiO2 could get as high as 100%)
    • then BiPAP (in addition to be able to provide 100% FiO2, the mask creates positive pressure upon inspiration and expiration to enhance air flow to facilitate gas exchange)
    • then intubation with mechanical ventilation support as the last resource


  • For patients with metabolic problems, the treatment is usually more straight-forward. In patient with metabolic acidosis, sodium bicarb is the primary treatment to increase the base to bring pH back to normal (sodium bicarb IV push first then continuous infusion). Bicarb is only used when pH <7.1 and HCO3< 6 mEq/L (Ellis, 2015) . According to Myra Ellis, there are two causes of metabolic acidosis, a real HCO3 deficit (which usually caused by kidney failure) or a net addition of strong acids (such as toxins, lactic acid in sepsis, or ketone in DKA) (Ellis, 2015). Bicarb replacement is only used for patient with true bicarb deficit (Ellis, 2015). In addition for patients with kidney injury, fluid challenge and diuretic therapy for patient with pre-renal kidney injury, hemodialysis for patient with intrarenal kidney injury or acute tubular necrosis (ATN). In patient with metabolic alkalosis caused by dehydration, fluid resuscitation is the primary treatment.

So far, we have learned how to correctly interpret ABGs as well as being able to understand their pathology and modalities. I hope that you find this helpful as you studying or working on the floor. If there is any discrepancy between what you read in my article and your text book, please don’t hesitate to leave me a comment below. I would love to hear from you.

Best Regards,



Ellis, M. F. (2015). Use of Bicarbonate in Patients With Metabolic Acidosis [Abstract]. Critical Care Nurse, 35, 5, 73-75. doi:10.4037/ccn2015502


Two Easy Steps to Know All Vasopressor Drips for New Nurses in the ICU

Hi everyone,

Today I would like to share with you two easy steps to be competent in all vasopressor drips in the ICU. If you are a brand new nurse who hope to land an ICU job fresh out of nursing school by impressing the ICU director during the interview, this article is for you. If you are a veteran ICU nurse who need some refreshment, this article is for you also. I hope you find this helpful in your daily practice as much as I do when I study to prepare to write this article. From the bottom of my heart, I hope to present this information as accurate as possible. Yet, if there is any discrepancy between what you read in my article and your text book, please don’t hesitate to leave me a comment below. I would love to clarify it with you with my best capability. Without further ado, Lets learn about the vasopressor drips and start saving lives.

Most of us probably already known what vasopressors is and how they affect the body, the blood pressure specially. Let’s break it down. Vaso (means vessels/blood vessels) pressor (means constricted). By definition, vasopressor is medication that constricts the blood vessels to increase blood pressure in hemodynamically unstable patients.

There are only a handful of vasopressor drip medications which you will encounter for the rest of your nursing career.  Those medication include norepinephrine (Levophed), dobutamine, dopamine, vasopressin, and phenylephrine (Neo Synephrine or Neo for short). To be able to understand why a physician prescribed dopamine but not norepinephrine in patients with cardiogenic shock, we need to know each medication and its mechanism.  There are two easy steps to know all your vasopressor drips:

  • You need to know the receptor sites and how they affect on the body
  • You need to know what receptor sites each medication target on

Step 1: There are many receptor sites in the our body, we are only going to discuss about Alpha 1, Alpha 2, Beta 1, Beta 2, Vasopressin (V1) and dopamine receptors:

  • Alpha 1 Receptors: located mainly in the peripheral blood vessels which have sympathetic properties thus cause vasoconstriction.
  • Alpha 2 Receptors: an antagonist with Alpha 1 Receptor which cause dilatation in peripheral blood vessels. For the purpose of this article, you don’t need to memorize Alpha 2 Receptors.
  • Beta 1 Receptors: located mainly in the heart which have sympathetic properties thus cause vasoconstriction mainly in the heart.
  • Beta 2 Receptors: located mainly in the bronchioles of the lungs and the arteries of the skeletal muscles. Beta 2 Receptor cause vasodilation in peripheral blood vessels.
  • V1 Receptors: located mainly in the peripheral blood vessels and cause vasoconstriction. They also located in vascular and GI smooth muscle with an anti-diuretic effect.

Before moving to step 2, I suggest you taking sometimes to be familiarize with those receptors.

Steps 2: Now that you know which effect each receptor has, let’s move on specific mechanism of each drug:

  • Norepinephrine (Levophed) affects on Alpha 1 and Beta 1 receptors thus it cause peripheral vasoconstriction and vasoconstriction in the heart to increase cardiac output. Norepinephrine is the most popular vasopressor drip drug because it affects both the heart and peripheral system. Norepinephrine is widely used in patients with septic shock or unknown types of shock. Norepinephrine can cause reflex bradycardia if you increase the doses too quickly. Dosage 2-30 mcg/min.
  • Dopamine affects on Alpha 1 and Beta 1 receptors thus it causes peripheral vasoconstriction and vasoconstriction in the heart. It has the same receptor sites as norepinephrine but is used with different purpose. Dopamine affects mainly on the Beta 1 receptors which is in the heart, thus it increase contractility and cardiac output. With that property, Dopamine is mainly used for patients with cardiogenic shock. With the same token, it is not a drug of choice for patients with elevated heart rate. Norepinephrine or phenylephrine (Neo) may be a better option. Dosage 2-20 mcg/kg/min.
  • Dobutamine affects in Beta 1 and Beta 2 receptor. Similar to Dopamine, Dobutamine mainly cause vasoconstriction in the heart. However, due to its Beta 2 property, Dobutamine can cause vasodilation in peripheral blood vessels. Dobutamine is also used in cardiogenic shock. Dosage 2-20 mcg/kg/min
  • Phenylephrine (Neo) affects in Alpha 1 receptors thus it does not have any control of the heart. Because it is purely peripheral vasoconstrictor, (Neo) is mainly used in neurogenic shock. Dosage 25-300 mcg/min.
  • Vasopressin affects on V1 receptor which causes peripheral vasoconstriction. Due to other effects on vascular and GI smooth muscle, Vasopressin is rarely used (or at least in my facility). Dosage 0.03-0.06 units/min.

As you learn about vasopressor drips, I suggest you review the four types of shock also. If you understand the causes, it will make more sense as you tie in the treatment with the condition patients have.

Below is youtube video from Strong Medicine Channel of Dr. Eric Strong.