Did you know?

Did you know that Amiodarone can prolong the QT interval?  Therefore, for Torsades it is not recommended.  Magnesium Sulfate is your recommended drug of choice.

Can you see what happened?

Can you see what happened in this EKG?

SHAMPOO

Here is a neat little patient assessment acronym to throw in your bag of tricks: SHAMPOO.

S - signs/symptoms
H - history of present illness
A - allergies
M - medications
P - pertinent past medical history
O - oral intake
O - ovarian cycle (if applicable)

Do you have any other acronym's not commonly used in EMS?

Heart Rhythms

Having trouble with your heart rhythms? Hopefully his can help.

I got this through a friend. I do not know the source for this image. If you know please share.

Pulmonary Embolism

The differential diagnosis of chest pain can include many conditions including angina, myocardial infarction, costochondritis, and pulmonary embolism.  In this article we are going to be looking at the field diagnosis and treatment of a pulmonary embolism.

Background

A Pulmonary Embolus occurs when a clot gets stuck in an artery in the pulmonary vasculature.  Clots can be caused from blood, fat, bone marrow, tumor fragments, amniotic fluid, or air bubbles.  These clots can affect preload to the left ventricle and/or oxygenation of the blood.

Incidence

More than 600,000 cases reported each year.  60,000 deaths within the first 4 hours.  Leading cause of death in hospitals.  Often times they are missed on initial presentation and found only on autopsy.

Signs and Symptoms

• Sudden death

• Pleuritic chest pain/chest wall tenderness (from distension of the pulmonary arteries)

• Hypoxia (lack of oxygenated blood returning to the heart)

• Hypotension (due to poor venous return to left ventricle)

• Tachycardia (to compensate for the decreased preload and to maintain cardiac output)

• Tachypnea (to compensate for hypoxia)

• Clear lung sounds

• Cyanosis around the nose and mouth (due to hypoxia)

• Dysrhythmias (PVC’s and Atrial Fibrillation)

• Leg swelling and tenderness (indicative of DVT)

• Friction rub

• Syncope (decreased cardiac output)

Field Diagnosis

• History

- Recent surgery or childbirth

- Immobility (bedridden patients, previous history of long travel)

- Certain medications (e.g. birth control)

- Hereditary coagulation disorders

- Smoking

• 3 Lead EKG:  Sinus Tachycardia

• 12 Lead EKG: “S1Q3T3”  Large S wave in Lead 1, Q wave in lead 3, inverted T wave in lead 3.  Other EKG findings include: ST Depression may noted in lead II.  Right atrial enlargement may also be noted in Lead II and V2.  T wave inversion in V1 through 4.  There may also be a right bundle branch block.

• End Tidal CO₂: hyperventilation with normal or high EtCO₂ levels.  Patients who are suffering from anxiety will demonstrate hyperventilation with low EtCO₂ levels.

Treatment

• High flow oxygen

• Ensure adequate tidal volume and provide ventilations if needed

• Cardiac monitoring

• Obtain IV access

• Alert receiving facility

Here is an example of the S1Q3T3

Works Cited

Brandt, P. (2010, December). Capnography Basics. Jounral of Emergency Medical Services , 6.

Dubin, D. (2000). Rapid Interpretation of EKG's. Fort Myers, FL: Cover Publishing Company.

Dalton, A., Limmer, D., Mistovich, J., & Werman, H. (2007). Advanced Medical Life Support. Upper Saddle, NJ: Pearson Prentice Hall.

Gould, B. (2006). Pathophysiology for Health Professions. Philadelphia, PA: Saunders Elsevier.

Dopamine Made Easy (hopefully)

Dopamine is a challenge to calculate for any Paramedic student.  The big problem that students have is that Dopamine must be calculated.  So the first thing to know is that Dopamine is based on μg/kg/min.

For the first example we will use:

• 400 mg of Dopamine

• 500 cc bag (either NaCl or D₅W depending on protocol/system)

• 75 kg patient

• Dose of 5 μg/kg/min

You should first notice there is an issue with the Dopamine in this example.  Its units are in mg but the equation is in μg.  This is easy to fix; multiply 400 x 1,000 (or just add three zeroes to the end of 400).  Now we have 400,000 μg.

When giving any medication, we need to know the concentration of the drug we are giving.  To find this take the amount of Dopamine we are going to give (400,000 μg) and divide it by the amount of fluid we have on hand (500cc).  This comes out to 800 μg/cc.  So in one cc of fluid we have 800 μg of Dopamine.

So lets rewrite the equation into something that we can plug into our phone/calculator that we may have on scene with us.  First rewrite the dose of Dopamine.  Get rid of the /’s and replace them with x.  So our new equation should look something like this: μg x kg x min.  Now, to get this new equation to work, we need to add one little thing: /concentration.

Our final equation should now be μg x kg x min / concentration.  In other words; the dose we want to give, multiplied by the weight of the patient in kilograms, multiplied by our drip set (which will be 60 drips in one minute), divided by the concentration that we calculated earlier (800 μg/cc).  Lets plug everything in:

5μg x 75kg x 60drips/min / 800μg/cc

This may look a little bit confusing so lets drop the units and we get:

5 x 75 x 60 / 800

And the final answer is 28.125 drips/min.  In other words you give this patient 28.125 drops every minute or 0.46875 drops every second.  Lets make life easy and do some rounding.  So you would give about 28 drops per minute, which would equate to about 1 drop every 2 seconds.

Lets take a look at another example.

• 250 mg of Dopamine

• 100 cc bag

• 125 kg patient

• Dose of 10 μg/kg/min

- First we need to get our Dopamine in the right units.  250mg x 1000 = 250,000 μg.

- Now find the concentration.  250,000 μg / 100cc = 2,500 μg/cc.

- Remember the new equation? Here it is again μg x kg x min / concentration.

10 x 125 x 60 / 2,500

- And we get 30 drips/min.

So lets say that as you were checking out your ambulance for the day and you forgot to stock your 60 drip sets and on your first call you need to give Dopamine.  Now what do you do.  We will use the following parameters:

• 400 mg of Dopamine

• 250 cc bag

• 125 kg patient

• Dose of 15 μg/kg/min

- First get the units correct: 400mg x 1,000 = 400,000 μg.

- Next find the concentration: 400,000 μg / 250cc = 1,600 μg/cc

- Use the new equation, but with one thing different.  Instead of 60 replace it with the drip set you are using (e.g. 10 or 15 in most cases).

- 15 x 125 x 15 / 1,600 = 17.578125 drips per minute using a 15-drip set.   We can round this to 18 drips per minute.

Lets take a look at one more example.

• 400mg of Dopamine

• 500 cc bag

• 150 kg patient

• Dose of 12 μg/kg/min

- First get the units correct: 400mg x 1,000 = 400,000 μg

- Next find the concentration: 400,000 μg / 500cc = 800 μg/cc

- Use the new equation: 12 x 150 x 60 / 800 = 135 drips/min

In this last example your bag will pretty much be running wide open to meet the needs of the patient.  This should demonstrate how important it is to use a medication pump, because all the calculations can be performed for you.

Eclamptic Seizure vs. Break Through Seizure

There are many causes of seizures and the treatment for seizures relies on treating the underlying cause.  For example, patients who are hypoglycemic may have seizures, which are corrected by the administration of Dextrose; patients who are hypoxic may have seizures, which are easily corrected by maintaining an airway and providing oxygen and ventilatory support; and for patients who are pregnant they may be suffering from eclampsia, which is treated by the administration of Magnesium Sulfate.  However, is Magnesium Sulfate indicated for the pregnant patient who is seizing and has a history of seizures and the medical provider is unsure if this is due to eclampsia or their known seizure condition?

Seizures are defined as “a brief alteration in behavior or consciousness,” which is “caused by abnormal electrical activity of one or more groups of neurons in the brain.”  While this is not fully understood, most believe that the “abnormal electrical activity” is often due to “a structural lesion or problems with brain metabolism,” which leads to “changes in the brain cell’s permeability to sodium and potassium ions.”  As the brain begins to struggle with changes in sodium and potassium, “the neurons’ ability to depolarize and emit an electrical impulse sometimes results in seizure activity”  (Sanders, 2007).

So how are seizures related to pregnancy?  After 24 weeks gestation, the mother may experience toxemia of pregnancy, also known as preeclapsia or the more severe form eclampsia.  Most often preeclampsia and eclampsia are “characterized by vasospasm, endothelial cell injury, increased capillary permeability, and the activation of the clotting cascade,” which often leads to the classic triad of preeclampsia:

• Hypertension (“blood pressure greater than 140/90 mmHg, an acute rise of 20 mmHg in systolic pressure, or a rise of 10 mmHg in diastolic pressure over prepregnancy levels.”)

• Proteinuria

• Excessive weight gain

Eclampsia incorporates this triad, however it also involves seizures or coma.  These signs and symptoms are often a “result from hypoperfusion to the tissue or organs involved;” and in the case of eclampsia, the brain, which is why seizures are seen (Sanders, 2007).

The treatment for eclampsia involves managing the seizures.  Diazepam or Lorazepam may be administered in conjunction with providing proper oxygenation and treating reversible causes (e.g. hypoglycemia).  In the presence of preeclampsia or eclampsia Magnesium Sulfate is administered (Sanders, 2007), but what if the seizing pregnant patient has a history of seizures and it is unknown if the patient is suffering from a preeclamptic seizure or a breakthrough seizure?  Should Magnesium Sulfate still be administered?  Sadeh et al. (1991) reports that research has shown “Magnesium Sulfate in acute uncontrolled generalized seizures” has had success in stopping the seizures in the patient presenting with status epileptics.

Sadeh et al. present a case in which a 16-year-old girl was admitted to the hospital for simple partial seizures, which soon turned into tonic clonic seizures.  The patient was treated with Phenytoin, but the seizures still persisted the patient was placed on a Magnesium drip.  While the patient was on the drip seizures did not occur; however, because the patient stayed into a deep coma and there was “generalized flaccidity and areflexia of the lower limbs the Magnesium Sulfate infusion was discontinued.”  Soon after the discontinuation of the Magnesium Sulfate, the seizures began to reappear, which prompted the doctors to place the patient back on the Magnesium Sulfate drip and once again the seizures stopped.  Over the next few days, the patient was taken off the Magnesium drip, which resulted in the seizures reoccurring and soon put back on the Magnesium drip, which would soon stop the seizures.  Sadeh et al. conclude that the use of Magnesium Sulfate as an anticonvulsant may be a better alternative to seizure therapy in patients experiencing seizures of unknown or specific etiologies.  Beck (2002) supports this claim made by Sadeh et al. by saying “[Magnesium Sulfate] depresses the CNS and controls convulsions by blocking [the] release of acetylcholine at the myoneural junction.”  Furthermore, Magnesium Sulfate “decreases the sensitivity of the motor end plate to acetylcholine and decreases the excitability of the motor membrane.  In fact, over 60 years ago Magnesium Sulfate was used to treat seizures of many etiologies including “uremic seizures and status epileptics as well as eclampsia … however with the advent of newer antiepileptic drugs its employment has been virtually limited to [eclampsia]” (Sadeh, Blatt, Martonovits, Karni, & Goldhammer, 1991).

Seizures, whether they are eclamptic or breakthrough, can be damaging to both the mother and the unborn child.  Because patients who are seizing often do not receive proper oxygenation to the tissues, establishing and maintaining an open airway is critical to the outcome of the patient.  Once an airway is established proper pharmacological drugs can be used to break the seizure.  Furthermore, eclampsia is associated with hypertension that can be deadly to the unborn child.  Whether or not it is known if the seizing pregnant patient is seizing because of a prior seizure condition or eclampsia, they should be treated as worst case scenario and Magnesium Sulfate should be administered because of its anticonvulsant effect, it “has a benefcial effect on factors leading to eclampsia,” and because it “can reverse arterial vasocontriction” (Wyllie, Gupta, & Lachhwani, 2006).

Works Cited

Beck, R. (2002). Drug Reference for EMS Providers. Albany, NY: Thompson Learning, Inc.

Sadeh, M., Blatt, I., Martonovits, G., Karni, A., & Goldhammer, Y. (1991). Treatment of Porphyric Convulsions with Magnesium Sulfate. Epilepsia , 32 (5), 712-715.

Sanders, M. (2007). Mosby’s Paramedic Textbook (3rd Edition ed.). St. Louis, Missouri: Elsevier Mosby.

Wyllie, E., Gupta, A., & Lachhwani, D. (2006). The Treatment of Epilepsy. Philadelphi, PA, USA: Lippincott Williams and Wilkins.

CHF Background and Treatment

The heart constantly has to beat in order to meet the metabolic demands of the body, however, in approximately 5 million people in the United States “the heart is unable to pump blood at a rate to meet” these metabolic demands.  This inability for the heart to pump blood effectively results in congestive heart failure, which leads to an impaired ventricular function and is often caused by “volume overload, pressure overload, loss of myocardial tissue, and impaired contractility”  (Sanders, 2007).  Although congestive heart failure is often associated with left ventricular failure, the right side of the heart can fail as well.  Because right and left heart failure affects different areas of the heart, patients may present differently depending on which side is affected.

When the left side of the heart fails to work as an effective forwards pump, left ventricular failure occurs.  As blood gets “delivered to the left ventricle,” it cannot be fully ejected from the ventricle, leading to a “back-pressure of blood into the pulmonary circulation.”  This causes an “increase in end-diastolic blood volume [which] increases left ventricular end-diastolic pressure,” which leads to fluid being backed up into the left atria and then into the pulmonary veins and capillaries.  Because the “pulmonary capillary hydrostatic pressure increases, the plasma portion of blood is forced into the alveoli,” which causes the plasma to mix with air leading to the “typical finding in pulmonary edema: foamy, blood-tinged sputum.”  This “foamy, blood-tinged sputum” can build up leading to hypoxia and eventually death (Sanders, 2007).

Because “left ventricular failure results in a reduction of stroke volume,” the signs and symptoms of left ventricular failure are often compensatory in nature.  Respiratory distress may be seen as patients become more hypoxic.  As hypoxia begins to set in, the blood pressure becomes elevated and the pulse rate becomes rapid to “compensate for low stroke volume.”  As hypoxia gets worse, the patient may have an altered level of consciousness because of poor cerebral perfusion and if hypoxia is severe enough, cyanosis maybe evident.  As the frothy sputum begins to accumulate the patient may begin to cough this up.  The frothy sputum also leads to adventitious lung sounds including: bilateral crackles “present at the base of the lungs and up to the level of the scapulae;” rhonchi from “fluid in [the] upper airways;” and wheezing from the “airway reflex spasm” (also known as cardiac asthma).  Jugular vein distension may also be seen which indicates a “back-pressure through the right heart and into the venous system.”  However, many of these compensatory mechanisms “often increase myocardial oxygen demand,” which “further [decreases] the ability of the myocardium to contract,” therefore, patients who present “with pulmonary edema (particularly those with an abrupt onset) also should be suspected of having an acute myocardial infarction” (Sanders, 2007).  Furthermore, patients may have “cardiac dysrhythmias such as atrial fibrillation or premature ventricular contractions” and complain of a recent history of “exertional dyspnea, paroxysmal nocturnal dyspnea, [or] orthopnea” (Ma, Cline, Tintinallu, Kelen, & Stapczynski, 2004).

In managing left sided heart failure, the goal is multifacitied, which includes “decreasing the venous return to the heart, improving myocardial contractility, decreasing myocardial oxygen demand, improving ventilation and oxygenation, and rapidly transporting the patient to a medical facility.”  When treating such patients; simple, non-invasive treatments can make a great difference in the outcome.  Applying high concentration oxygen ensures that every red blood cell is fully oxygenated and allowing the patient’s legs to hang off of the gurney while assuming a sitting position increases the capacity of the lungs, which aids in the work of breathing and “decreases venous return to the heart.”  If non-invasive treatments do not work, more aggressive management may be needed, such as positive pressure assistance to help decrease pulmonary edema and also reduces “the need for high levels of inspired oxygen.”  If cerebral hypoxia or progressive hypercapnia exist, or if the patient is unable to maintain a SpO₂ reading greater than 90% with 100% oxygen, endotracheal intubation may be required (Sanders, 2007).

Once the airway is under control, an intravenous line may be established and pharmacological agents such as Nitroglycerin, Furosemide, and Morphine administered to “decrease venous return, enhance contractile function of the myocardium, and reduce dyspnea.”  Nitroglycerin helps patients in congestive heart failure by reducing peripheral vasodilation which leads to a reduction in “preload and afterload, thereby reducing the myocardial workload and improving cardiac function.”  Furosemide supplements Nitroglycerin by relaxing the venous system, which has a dilating effect that occurs within five minutes.  Furosemide also reduces the intravascular volume by having a diruetic effect,   however, this diuretic effect of Furosemide may lead to electrolyte imbalances.  Morphine is used to reduce preload on the heart by decreasing the venous return by dilating “the capacitance vessels of the peripheral venous bed” and to reduce the work of the myocardium and anxiety  (Sanders, 2007).  It is important to note that the use of Morphine in the patient who is undergoing a CHF exacerbation is controversial.  As the patient becomes hypoxic, Morphine may enhance the hypoxia by causing respiratory depression.  Furthermore, it is believed that Morphine has very little benefit to the patient when compared to oxygen, diuretics, and nitrates  (Ma, Cline, Tintinallu, Kelen, & Stapczynski, 2004).  Furthermore, Morphine, as well as Nitroglycerin and Furosemide, lower the blood pressure; therefore the use of these medications should be used with caution or not at all in patients who have a systolic blood pressure less than 100mmHg (Sanders, 2007).

If the right ventricle of the heart “fails as an effective forward pump,” then right sided heart failure occurs which causes a “back-pressure of blood into the systemic circulation.”  If this back pressure gets too high, it can result in “the plasma portion of blood [being] forced out into the interstitial tissues of the body,” thus resulting in edema, “particularly in the dependant areas of the body” (Sanders, 2007).

As the right side of the heart begins to back up, various signs and symptoms may develop in other parts of the body.  Most often tachycardia is present.  Venous congestion, leading to an “engorged liver, spleen, or both” may be noted.  As the fluid begins to build up, edema may be seen in the lower extremities or “sacral region in bed ridden patients.”  Fluid may even build up in the abdomen leading to ascities or in the pericardium leading to pericardial effusion.  Often right sided heart failure is the result of left sided heart failure, therefore signs of left sided heart failure may be present as well.  Furthermore, patients may have had a previous myocardial infarction along with taking medications such as digitalis or diuretics (Sanders, 2007).

Right sided heart failure is often considered a chronic condition, therefore, it rarely presents itelf in the prehospital environment.  However, there are times in which right sided heart failure may be “associated with pulmonary edema or hypotension,” thus making it a medical emergency.  Treatment for right sided heart failure is mainly supportive.  Allowing the the patient to maintain a position of comfort, normally in a sitting position; along with maintaining an open airway with high concentration oxygen may be all that is necessary to treat such patients.  In the presence of hypotension, starting an intravenous line and administering fluid may “help normalize left ventricular filling.”  If hypotension is not present, an intravenous line may be established to keep the vein open.  Further treatment for the patient in right sided heart failure also includes treating left sided heart failure in the event it is present (Sanders, 2007).

When treating a patient in heart failure, one must also take into account other causes of respiratory distress including, “asthma, chronic obstructive pulmonary disease, pneumonia, pulmonary embolus, allergic reactions … [and] noncardiac pulmonary edema such as drug-related alveloar capillary damage or that seen with acute respiratory distress syndrome.”  Furthermore, certain “causes of pulmonary edema need to be determined rapidly because they require emergency intervention.”  Acute myocardial infarction should always be considered as a possible cause of congestive heart failure exacerbation as it is often seen in left sided heart failure.  Acute mitral valve or aortic valve regurgitation should also be considered as the patient may require surgery; however, prehospital providers will have no way to determine this unless the patient has a known history of these conditions.  If dysrhythmias or electrolyte imbalances exist, they should be treated, however, “those therapies that impair the inotropic state of the heart should be avoided” (Ma, Cline, Tintinallu, Kelen, & Stapczynski, 2004).

Regardless of which side of the heart is affected, all patients undergoing a CHF exacerbation should receive high concentration oxygen and be allowed to maintain a position of comfort while enroute to the hospital.  Furthermore, vitals signs and an electrogradiogram, along with a complete patient examination and a focused history should be performed.  Complications associted with a CHF exacerbation should be treated using local protocols.

Works Cited

Ma, J., Cline, D., Tintinallu, J., Kelen, G., & Stapczynski, S. (2004). Emergency Medicine Manual(6th Edition ed.). The McGraw-Hill Companies, Inc.

Sanders, M. (2007). Mosby’s Paramedic Textbook (3rd Edition ed.). St. Louis, Missouri: Elsevier Mosby.

Hepatic Encephalopathy

As the largest internal organ in the body, the liver is responsible for many functions including iron metabolism, plasma-protein production, and the detoxification of drugs and other materials (Sanders, 2007).  Once the liver fails, it is unable to neutralize toxins, which then start to build up.  These toxins “escape through the intestines and enter the systemic circulation, causing neurochemical changes in the brain.”  These neurochemical changes in the brain, as a result of liver failure, are known as hepatic encephalopathy or portal-systemic encephalopathy.  It is believed that “the accumulation of unmetabolized toxins (primarily ammonia) in the brain, false neurotransmitters, and neuroinhibitory substances are believed to be the main mechanisms of [hepatic encephalopathy]” (de Melo, Charneski, & Hilas, 2008).

Most often hepatic encephalopathy is seen in patients who suffer from cirrhosis of the liver.  In fact, it is estimated that 50-70% of patients who present with hepatic encephalopathy are a result of cirrhosis of the liver.  Besides the patient’s medical history, patients who are suffering from hepatic encephalopathy will also present with signs and symptoms that resemble impairment of the brain (de Melo, Charneski, & Hilas, 2008).  Altered mental status, hepatic coma or coma hepaticum, cerebral edema, and death are commonly associated with hepatic encephalopathy.  Early in the disease process some patients may have a “day-night reversal,” in which the patient sleeps during the day but stays awake at night (Wikipedia).  Some patients may also experience dementia, spastic paraparesis, cerebellar degeneration, or extrapyramidal movement disorders, which the clinician may attribute to another cause besides hepatic encephalopathy (de Melo, Charneski, & Hilas, 2008).  According to Wikipedia, “the hallmark of hepatic encephalopathy on the physical examination is the presence of asterixis;” which is a tremor in the patient’s wrists while patient’s arms are outstretched and the wrist is extended.  Some have said this resembles “a bird flapping its wings” and it is believed this is due to the inability of the liver to metabolize ammonia to urea.  However, asterixis may also be seen in “states such as renal failure and carbon dioxide retention” (Wikipedia).

In the prehospital environment, not much can be done for the treatment of hepatic encephalopathy.  Prehospital treatment is primarily supportive care because treatment is long term through the use of medications and diet, which “focus on the resolution of ammonia accumulation and identification/removal of precipitating factors.”  Currently Lactulose is used in the treatment of hepatic encephalopathy, however other drugs, such as Rifaximin, are being studied for the use in hepatic encephalopathy.  For patients who are being treated using diet, “protein should be restricted and uresase-producing colonic bacteria should be inhibited” (de Melo, Charneski, & Hilas, 2008) (de Melo, Charneski, & Hilas, 2008).

Works Cited

de Melo, R., Charneski, L., & Hilas, O. (2008). Rifaximin for the Treatment of Hepatic Encephalopathy. American Journal of Health-System Pharmacy , 65 (9), 818-822.

Sanders, M. (2007). Mosby's Paramedic Textbook (3rd Edition ed.). St. Louis, Missouri: Elsevier Mosby.

Wikipedia. (n.d.). Asterixis. Retrieved August 4, 2008, from Wikipedia: http://en.wikipedia.org/wiki/Asterixis.

Wikipedia. (n.d.). Hepatic encephalopathy. Retrieved August 3, 2008, from Wikipedia: http://en.wikipedia.org/wiki/Hepatic_encephalopathy.