Tag Archives: PCCN

Help!

13 Apr

Help by Fellow World

Click on the art to credit the artists.

Help me, I am stuck in that tree.  April 21 I will be taking the PCCN cert exam. I am a good test taker, I can eliminate the wrong answers. I can do that.

It is kind of like knowing what you do not want, but never knowing what you do want.

Somebody help me. It is cold and cloudy, and I just can’t sit any longer. Please tell me I am not all alone in this!

Just what does Potassium 3.5-5.0meQ/L do? it maintains intracellular water and acid/base balance.

Hyperkalemia is usually caused by renal failure. The symptoms of this may be bradycardia, tremors, twitching, tall peaked T waves. The treatment is: Kayexelate, dialysis, insulin/D50, or HCO3/Ca++.  It can take a while for the Kayexelate to work. I once had a patient NPO and the nephrologist actually wanted me to give the Kayexelate via rectal enema.When I asked him how was I supposed to keep the medicine in the rectum long enough for it to work, he told me to use a “butt cork”!  I bothered him till he cancelled that request and changed his mind to give HCO3.

Hypokalemia can be caused by inadequate intake or renal loss. NPO patients should be getting KCl 40meQ each day somehow. The symptoms are tachycardia, hypotension, flaccid muscles, and flat T waves. The treatment is: give KCl orally preferably, or IV.

Calcium 8.4-1.2mg/dL is needed for the contraction of the heart and blood vessels and coagulation.

Hypercalcemia is caused by bone loss or destruction. The symptoms are coma, flaccid muscles, short ST and QT interval. The treatment is IV fluids, diuretics and phosphate.

Hypocalcemia is caused by a low albumin, multiple blood transfusions. The symptoms are seizures, laryngeal spasm, hypotension, flat ST, and a small T wave. The treatment is calcium gluconate.

Magnesium 1.5-1.95meQ/L , my most favorite electrolyte of all! It is needed for the relaxation of the heart and blood vessels and it is NEEDED for the absorption and utilization of other electrolytes. Stop running those K riders, if the Mg is low you are wasting time and burning the veins if you do not replace the MG too! We like the Mg above 2! ❤

Hypermagnesemia is caused by renal failure. The symptoms are CNS depression, hypoactive reflexes, bradycardia, and hypotension. It is treated by giving IV calcium.

Hypomagnesemia is caused by inadequate intake. The symptoms include irritability, increased reflexes, ST depression, and T wave inversion. The treatment is Magnesium. I think I will go take some oral Mg right now.

Phosphorous 2.5-4.7mg/dL is essential for ATP production. Our cells need that energy.

Hyperphosphatemia is caused by renal failure. The symptoms are asymptomatic but you will see a low calcium. The treatment in Amphogel, Insulin/D50, Dialysis, Fluids.

Hypohosphatemia is caused by Mg deficiency, re-feeding syndrome, acute respiratory distress. The symptoms look like a decreased level of conciousness, respiratory distress, muscle weakness. The treatment is: phosphorus.

Sodium 135-145mEq/L is needed for water movement and the changes may cause cerebral edema.

Hypernatremia is caused by fluid loss. The symptoms are thirst, and CNS depression. The treatment is free water D5W. If they have a PEG tube you will be shoving in tap water bolus.

Hyponatremia is caused by overhydration with IV fluids sometimes. The symptoms are edema and mental status changes. The treatment is a fluid restriction, normal saline, or hypertonic saline. I was so afraid to run hypertonic saline the first time. The patients sodium was like 109.

The medications on the PCCN test with the desired effects!

Let’s make it easy!

All of the following medications increase the heart rate, the blood pressure and the cardiac output, these winners are:

Dopamine 2-20 ug/kg/min- Dobutamine 5-15ug/kg/min–Levophed 2-12 ug/kg.min–Epinephrine 1-10ug/min

Got that? OK give me some LOVaphed, will that be on the test? I know about that drug.

The next medication Digoxin 0.125-o.5mg will decrease the heart rate, actually increase the blood pressure (diastolic especially but don’t quote me on that) and increase the cardiac output.

The Nitroglycerine 5-20ug/min does nothing to the heart rate, it decreases the blood pressure and can either increase or decrease the cardiac output.

The Nitroprusside 0.1-10ug/kg/min increases the heart rate, decreased the blood pressure and cardiac output.

The Amiodarone Bolus 150-300mg followed by drip decreases the heart rate and blood pressure and increases the cardiac output. I have a love/hate relationship with Amiodarone.

Next!

Localizing the injury on the 12 lead EKG

Trouble: T wave inversion is ischemia. ST segment elevation is injury and Q waves indicate necrosis.

First find out if the changes are in more than 1 lead or every lead.

Next!

The vessels LCD and the LAD affect the anterior heart, the changes are in lead V3, V4

The vessel RCA affects the inferior heart and the changes are in lead II, II, AVF And remember with an inferior wall MI we are supposed to get a right-sided EKG which I have never even seen before!

The vessels LCA and the Circumflex affect the lateral heart and the changes are in V5, V6, I, aVL

The vessels LAD and PDA affect the posterior heart and the changes are reciprocal in leads V1-V4

The RCA vessel also affects the right ventricle and is present in V4R

Go memorize.

Now for my favorite part where all of you are going to pee pee in your panties!

H20+CO2=H2CO3=H+HCO3

Water and carbon dioxide equals carbonic acid equals hydrogen and bicarbonate! <giggles>

I loved chemistry in nursing school. I almost changed course on the ship of academia, but I held onto nursing steadfast.

It is just a balancing act this acid base balance and our lungs and our kidneys are working hard at it, even if you do not feel it.

Maybe I feel it. I like HCO3 in my mouth when I brush my teeth with baking soda like the old days when there was no toothpaste in the medicine cabinet. Just dip your brush into a box of Arm and Hammer and rinse it out with hydrogen peroxide. I bet you will have white teeth just like me, even if my teeth are slightly crooked. I like them that way, but I better stop licking them with my tongue, I do not want to get subacute bacterial endocarditis or something.

Anyway on with the ABGs

pH 7.35-7.45

pCO2 35-45mmHg

pO2 80-100mmHg

O2 sat 95-100%

HCO3 22-26mEq/L

Base Excess + or -2

Forget about the Anion gap-that better not be on the test! If it is I will punch the computer module and walk out. Just kidding!

So we have the lungs that remove CO2 that is made by cellular processes. That is what the lungs do to balance the pH. The kidneys balance by producing HCO3 and by getting rid of H+ ions. The way these organs interact is via the making of carbonic acid H2CO3, which is a constant thing. The water will attach to carbon dioxide, then when needed this breaks apart to make hydrogen ions and bicarbonate.

It is just a continuous, compensating balancing act to keep the pH normal.

I doubt that chemistry will be on the exam so here I will put it to use.

1. A 60 year old liver transplant patient with pneumonia, a room air ABG reveals: pH 7.46 (alkalosis) CO2 32 (alkalosis) pO2 77 (hypoxemia) O2 sat 96% (normal) HCO3 23 (normal)

The patient is mildly hypoxic with uncompensated respiratory alkalosis. From the low pO2 the patient might be breathing faster, blowing off the CO2 causing this problem. There will probably not be any treatment for this at this time.

2. A 22 year old has been fasting to lose weight. She is a diabetic. Noone is sure if the patient has been taking the insulin at home for a couple of days. ABG goes like this

pH 7.20(acidotic) CO2 28 (alkalosis) pO2 96 (normal) O2 sat 96% (normal) HCO3-11 (acidosis)

The patient has partially compensated metabolic acidosis from DKA. The treatment is to correct the glucose with insulin and IV fluids. If the internal medicine doctor tells you to give bicarbonate: don’t do it! It will not fix the pH and will mask the underlying problem.

3. 60 year old with chronic renal failure complaining of dizziness. ABGs are drawn.

pH 7.37 (normal) CO2 34 (alkalosis) pO2 94 (normal) O2 sat 97% (normal) HCO3 19 (Acidosis)

Common to renal failure this is fully compensated metabolic acidosis. No treatment.

Pt admitted for COPD. ABG

pH 7.33 (acidosis) paCO2 60 (acidosis) pO2 75 (hypoxemia) O2 sat 94% (low) HCO3 31 (alkalosis)

This is partially compensated respiratory acidosis and the patient will probably get a BiPAP on telemetry!

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A pink frothy mess

13 Apr

My heart is failing and
Your fluid and my air
become together
A pink frothy mess.

I drown in your pink sea.

Acute pulmonary love edema.

Do you want to be the oxygen, or do you want to be the blood, or do you want to be oxygenated blood?
I wrote this poem before and put it here somewhere a few years ago, I just chopped it down a little bit. The lungs filled with water, and the crooked heart is my art above. I miss drawing, but I do not have the software corelDRAW anymore, so my days of being a fake artist are over. Besides my art work is not that great.
I can write fake love poems like the one above to go with fake art, but the thing is I better get studying. I test next Wednesday.
So the first time I experienced this acute pulmonary edema working on telemetry revealed some facts to me. I had learned about this in school probably, maybe not. What happened was that my patient during 0800 assessments appeared anxious, but was saturating fine according to the pulse ox and the blood pressure was high normal, although I noticed the diastolic seemed high, but not >1o0. His lungs sounded totally clear. He was a big guy sitting up with 3 pillows in the bed. He did not have massive edema or anything like that. I figured he would need some XANEX in the future.
Xanex is not what the patient needed. By the time 1200 assessments came around, the patient was labored, short of breath, with a respiratory rate around high 20s per minute. You see tissues all over the floor with ping tinged sputum, and wonder: Where the hell have I been for 4 hours?  The blood pressure was 200/110, and rales, tachycardia, and the patient was cool. The patient was desaturating to the 80s.  The patient was starving for air, you know that look in the eyes. That look from the patient, is like some kind of fear, that I do not want to ever feel. And then they want to talk and tell you about how they can’t breath, and we tell them, don’t talk, we already know, we are going to try to fix this right now.
I said, Uh-Oh this is not right. The work to breathe appeared so hard, people like that can not carry on with that workout forever. Ya know, the abdomen is swelling up and collapsing down hard with each breath. It really is a strange sight. The patient was given, oxygen, morphine, lasix, and hydralazine and guess what? It worked! And worked quicker than I thought it would. The patient was stabilized and stayed on telemetry.
Oh hell. I can not draw or write poems. Here are some pulmonary questions like the test questions. The answers are highlighted in blue.
1. The patient is 1 day post op from AAA repair. She develops atrial fibrillation with subjective dyspnea. The heart rate is 121 with normotension. What pulmonary complication might this be from?
a. Pneumonia
b. ARDS
c. Shock lung
d. Pulmonary embolism.
2.The patient is recovering from a right lower lobe lobectomy by VATS procedure. There is significant subcutaneous emphysema in her upper chest and neck area. As her nurse should recognize that which of the following is the highest priority?
a. Maintaining the airway
b. Assuring patency of the chest tube
c. Administering oxygen at 2 liters nasal cannula
d. Suction the airway as needed.
*apparently the emphysema travels upward by chemical nature and can put pressure on the airway. I have only felt those rice crispies once.
3. How does a D Dimer lab test help to diagnose pulmonary embolism?
a. positive test indicates PE
b. A negative test rules out PE
c. A positive test rule out PE
d. A negative test indicates PE
*That is right people, I made it bold blue for a reason. Elevated D Dimer does not mean PE!  Stop freaking out over the elevated D Dimer please.
4. The  patient was admitted for an acute stroke. The patient is alert but has left-sided weakness and is having difficulty swallowing. This morning the patient is short of breath and has rales in all lung fields. The most likely cause of this distress is
a. PE
b. Aspiration
c. Heart failure
d. Neurogenic pulmonary edema
* Swallow evaluation please, happens all the time. Stop feeding the acute stroke orally till the patient can swallow properly. ughhh
5.  The patient comes to the emergency department with an exacerbation of COPD. The patient is hypoxic and hypercapneic. The patient does not want to be intubated and does not want mechanical ventilation. What criteria are necessary to initiate bi-level postive-pressure ventilation (BiPAP)?
a. Must be able to slow down the breathing and not fight the machine
b. Must be able to maintain his own airway
c. Must be less than 75 years old.
d. Must quit smoking first
* And not be puking into the BiPAP mask. Also less than 48 hours.
6. Nursing interventions to decrease the rate of hospital acquired pneumonia include
a. Placing gastric tubes through the nose
b. Brushing the patients teeth
c. Administering systemic antibiotics
d. Keeping the patient NPO
*yeah oral care
I will inhale the rest of the pulmonary section tomorrow. I got lazy today.
I am going to dream about pink frothy messes sans respiratory distress.

You are dynamic

8 Apr

BrOkEn_HeArT____by_KillerkeksX

credit the artist: click on the art to be taken there.

Every girl should get the guy with the glue gun, to bond that broken heart back together, just like…Every patient in heart failure should get the Nurse walking to the room with the Lasix, getting ready to reduce that preload and diurese that patient.

Nothing makes me tickled more than giving Lasix 100mg, and watching that patient pee pee that light yellow liquid to get their volume off.  Just don’t forget the oral potassium.

Sometimes I just want to hold up the syringe and say: You go pee pee now. I do not cause that would not look professional, especially because I would most likely be laughing at the same time.

Cardiovascular, it is a fluid filled system, driven by a pump. We can assess what is going on with our patients without invasive hemodynamic monitoring, in a way. We do it all the time, even if we do not understand how it all relates.

I like the word dynamics. You are a dynamic person. It is definitely a positive adjective: change, progress, activity, full of energy. I like that.

Add hemo, plus dynamics and we have: the forces that circulate blood throughout the body. Hemodynamics, it has to be optimal for maintaining healthy organs. The 3 things we are assessing, non invasive, at the bedside are: the pump, the volume, and the resistance. That is the heart, the blood, and the vessels, respectively.

The power of the heart: inotropy or contractility. It is like how hard the heart has to pump a  volume of blood if the preload is increased, or how hard it has to pump against the resistance, that is the afterload to get it out to our bodies. So the things that affect this contractility are the fluid volume, the oxygenation of the heart and the resistance.

We are assessing the hearts power by, checking the heart rate, the systolic blood pressure, organ perfusion: mental status, kidney function; and peripheral perfusion: capillary refill and pulses.

The preload is the end diastolic volume. It is the blood volume in the ventricle to be ejected. If the preload is too high or too low, it makes the heart work harder, and increases the demand on the heart. An over stretched heart from too much preload has a reduced contractility, we do not want that.  There has to be a happy middle.

I know that the first time I ever saw a  JVD, it looked like a pulsating blue caterpillar crawling up the neck.  I ran out to the nurses station and was like, “Fave Cardio! My patients got blue caterpillars pulsating on the neck!” Now, 3 years later, I just say to myself, “Wow, that is some JVD, this patient in heart failure might have increased preload.”

What do we do to manipulate the preload? For heart failure patients we find ourselves giving diuretics to reduce the preload, we are reducing the volume that is getting back to the heart. Increased blood volume and a slow heart rate (more filling time) will increase the preload. Hypovolemia decreases the preload, and if necessary we give fluids to the patient. We are either giving fluids or taking them away to manipulate the preload. Since we are dealing with the venous here, that is 70% of our blood volume, we can alter the preload with drugs too! Yaay! We play with the venous holding tank when we give the drug Nitro, we are vasodilating and keeping the fluid out. To increase the preload by vasoconstriction, to bring the volume back to the heart, nurses in the ICU or ER are infusing Levophed.

I just take a hot shower to reduce my preload, and I just ask for some LOVaphed to increase my preload.

We assess the preload with those daily weights, strict intake/output monitoring and yes: the Jugular Veins.

The afterload is the resistance to moving the preload against the arterial vascular resistance.  It is the what the heart has to move the blood against. If the afterload is too high, it like a kinked tubing on the IV pump, it just does not get through well. The blood will back up from the pressure if the heart is weak and the patient will get into some heart failure. With a high preload, it is vasoconstricting, most likely from a that haywire compensatory system when the cardiac output drops: there goes the SNS again, vasoconstriction. The goal is to open it up, and get less resistance.

We assess this afterload with the diastolic blood pressure because that is when the heart is at rest and the only pressure maintained is that of the vessels themselves. When the resistance is high, we are seeing the patient that is cool, pale, and diaphoretic. And then we say, Uh-Oh now what do I do?

Surely, it is more complicated than this right? This is my understanding so far of hemodynamic monitoring of patients, in the place that is Telemetry, because that is where I spin every week.

We give drugs, take blood pressures and see the urine output.

Here are the last 14 cardiovascular questions I will type.

1. A sign of peripheral arterial occlusion

a. Pallor

b. Swelling

c. Redness

d. Dyspnea

* I had to deviate and highlight in blue

2. The patient just went to the unit after a carotid endartectomy CEA, the nurse will assess for all of the following except:

a. Hypertension

b. Change in mental status

c. Bleeding

d. Seizures

* that word except, the rest are common complications

3. A thoracic aortic aneurysm causes chest paint that

a. Radiates to the left arm

b. Bores through to the back

c. Is sharp and worse when laying down

d. Is associated with diminished breath sounds

* a=ACS, c=pericarditis, d= pneumothorax

4. Stabbing chest pain, that is worse in the supine position, with fever and chills is probably

a. Myocardial infarction

b. Pulmonary embolism

c. Pericarditits

d. Pneumothorax

* All kinds of chest pain

5. Management of pericarditis includes

a. Monitoring for signs of cardiac tamponade

b. Evaluating pain relief

c. Providing emotional support

d. All of the above

*Yes all.

6. Sub-acute bacterial endocarditis is usually caused by

a. Dental procedures

b. Normal valves

c. IV drug abuse

d. Prosthetic valves

*I really need to stop licking my own teeth all the time, seriously

7. The valve most affected by infective endocarditis is

a. Mitral

b. Aortic

c. Tricuspid

d. Pulmonary

8. The patient is recovering from an acute MI, he gets tachycardia and hypotension. You hear muffled heart sounds, and suspect

a. Pericarditis

b. Myocarditis

c. Pericardial tamponade

d. Reinfarction

* It is a triad coming up

9. Beck’s Triad of symptoms of cardiac tamponade are

a. Tachycardia, hypotension and muffled heart sounds

b. Rales, soft heart sounds, bradycardia

c. Widened pulse pressure, atrial arrhythmias

d. Hypertension, flushing, pulsus parodoxus

10. The patient comes to the ED after MVA with chest pain, dyspnea and has ST segment elevation on the anterior leads, the patient might be suffering from

a. Pneumothorax

b. Flail chest

c. Cardiac contusion

d. Pulmonary embolism

11. In cardiogenic shock the initial goal is

a. Increase the cardiac output

b. Increase the oxygen supply

c. Decrease oxygen consumption

d. Decrease contractility

*initially

12. The medication that increases oxygen supply to the heart during cardiogenic shock is

a. Dopamine

b. Nitrogylcerine

c. Nitroprusside

d. Dobutamine

*coronary vasodilator

13. Calcium channel blockers have which of the following functions

a. Increase vascular tone

b. Increase the velocity of the AV node

c. Decrease cardiac oxygen consumption

d. Increase cerebral oxygenation

*by blocking calcium uptake, it causes relaxation, slows down the heart, decreasing consumption also it decreases tone and velocity. How many times a working day do I say? Now here is your calcium channel blocker: swallow it, or give me your arm!

14. The patient has a Brain-Naturetic Peptide of 1273 (picograms/ml) you are the nurse and suspect

a. Acute ischemic stroke

b. Acute renal failure

c. Heart failure

d. Hip fracture

* this was first found in the brains of animals. The enzyme is produced by the heart to maintain fluid volume. When the heart is stretched from overload, the heart releases the enzyme, and it helps the renal system to dump off the fluid. The BNP > 500 is likely some kind of heart failure. How about when the BNP is > 5,000! Yikes.

This is it, no more questions till next week, I will be at the circus riot, I mean work for the next 3 shifts! I will be measuring the intervals and skating on IV poles.

I like it here, in your heart.

8 Apr

The title of this piece is Bored_in_Maths_by_Leohhx, if you click on the image you will be taken to the original artwork, on deviantART.  She might have been bored in Math class, while her friends were playing soccer. I am kind of bored studying for PCCN certification, but I only have a short time left so I am studying everyday.

I am still sucked into cardiac, like the sucking of blood into the ventricles. I keep getting sucked into right ventricle, I am trying to get oxygenated, trying to make into the pulmonary section, but the truth is: I like it just where I am. It is all about the pump for me.

The heart is a pump. I could write love-lorn poetry just for that pumping action, and for no other reason than that, I mean that is enough, right?

Don’t tell me your heart skips a beat when you see me, I will tell you that it is nothing more than a premature atrial contraction.

If my heart speeds up, it is nothing more than an overactive sympathetic nervous system warning me of the big bad wolf, or something like that.

Of course it is more than that, but for all my intents and purposes right now, the psuedo-love-heart-poems will have to wait.

10 more questions, the answers are underlined and highlighted in red. I doubt I will type the rationales.

1. The most common cause of a NEW S3 heart sound:

a. Cardiac tamponade

b. Papillary muscle rupture

c. Acute heart failure

d. Myocardial infarction

* i am bored

2. The most common type of aortic aneurysm is

a. Ascending

b. Aortic arch

c. Descending

d. Abdominal

* i am bored

3. Peripheral vascular disease can present with intermittent claudication. The pain from femoral-popliteal disease will be in the:

a. Calf

b. Waist

c. Thigh

d. Arm

* anatomy

4. Which condition would stimulate renin production:

a. Increased supply to the renal tubules

b. Decreased blood pressure

c. Decreased sympathetic output

d. Increased sodium retention

*yeap

5. Acute rejection in cardiac transplantation is diagnosed by

a. ECG

b. Chest X ray

c. Echocardiography

d. Endomyocardial biopsy

6. Cyanosis on exertion may be a sign of

a. Atrial flutter

b. Ventricular septal defect

c. Acute coronary syndrome

d. Pulmonary embolism

* not oxygenated

7. Patient is admitted with an anterior wall myocardial infarction. What 12 lead EKG changes do you expect?

a. T wave inversion is lead I and AVL

b. ST segment elevation in V3 and V4

c. QRS duration > 0.04 in all leads

d. Tall R waves in V6

* still memorizing EKG changes till I find a way to visualize

8. What additional diagnostic test must be done on all patients with an inferior wall myocardial infarction

a. Pulmonary function tests

b. Right sided EKG

c. Endoscopy

d. Continuous ST segment monitoring.

* I am thinking of the respiratory therapists about answer letter a! LOL

9. Oxygen therapy is recommended for all patients with Acute coronary syndrome for the first 6 hours after stabilization. The goal is

a. Keep oxygen saturation at 100%

b. Balance oxygen supply and demand

c. Reduce workload on the heart

d. Prevent pulmonary edema

10. Which reperfusion therapy is recommended as the initial treatment for patients with STEMI and a history of intracerebral bleeding?

a. Thrombolytics–tPA

b. Percutaneous coronary interventions

c. Coronary artery bypass grafting

d. AICD

*well surely not tPA!

And that concludes this session, I am so lonely with this studying. It must be obvious.

lonely PCCN

5 Apr

I need a pacemaker STAT

If you click on the image of this artwork you will be morphed to the artist of this fine idea, found on deviantART. The title of the piece is “Cardiac insufficiency” by Mariix.  I doubt the artist is a nurse, or a doctor, but she has the right idea: the heart needs juice, electrical juice that is.

Somebody plug me in please. I am a lonely student in my studies for PCCN certification. I need some joules.

Here I am studying for PCCN again. My test date is April 21, so I can not be lazy anymore.  Since it has been so long since I have really studied, I am starting back with cardiovascular, which is 46% of the exam equals 45 questions.

Some of the sample questions seem easy, some of the study material seems hard.

I have an undying opinion that telemetry nurses are special, and not just because I am one of them silly!  Of course I get tired of spinning tele packs, especially when the acuity is high and the ratio is just as high. I still have the energy to do it, so I keep on measuring the QTc.

So here are the first 10 easy sample questions, and I will summarize rationales. The answers are underlined and highlighted in red for  cardio-LOVE.

1. Which of the following variables affects the cardiac output directly?

a. Preload

b. Stroke Volume

c. Afterload

d. Resistance

*All the answers may affect the CO but only the SV does so directly. The way to increase the CO is to manipulate the SV (too much or too little venous return to the heart) and manipulate the HR (is it too fast or too slow?) I am obsessed with the manipulation of the heart.

2. Coronary artery perfusion is dependent upon

a. Diastolic pressure

b. Systolic pressure

c. Afterload

d. SVR

*Coronary arteries fill during diastole

3. The patient is short of breath with chest pain. The heart rate is irregular at 170 beats per minute and the blood pressure is low at 80/60.  Anticipate and get ready for the following:

a. Atropine 0.5mg IV

b. Labetolol 25mg IV

c. Cardioversion 100J

d. Lidocaine 75mg IV

* Atrial Fibrillation with a rapid ventricular response that is hemodynamically unstable. Conversion is either electrically or chemically but none of the other answers include drugs that could chemically convert rapid A fib, so the answer is cardioversion with 100J. I just did this last week at the bedside for an unstable situation and believe me: IT HURTS! The patient went into NSR and screamed: “Don’t ever do that again!”  Next time I will advocate for some Versed instead of just the Fentanyl.

4. Chest pain that is NOT relieved by rest and nitroglycerine is called:

a. Variant angina

b. Stable angina

c. Unstable angina

d. Prinzmetal’s angina

*No explanation, it is easy.

5. The nurse administering tPA for acute myocardial infarctions should monitor the patient for all these EXCEPT:

a. Peripheral thrombosis

b. Myocardial reperfusion

c. Bleeding complications

d. Coronary reocclusion

* self-explanatory: thrombosis will not occur in the periphery after tPA

6. Which finding would indicate coronary reperfusion during tPA infusion?

a. Drop in arterial blood pressure

b. Elevation of the ST segment

c. Ventricular fibrillation

d. Dramatic reduction in chest pain.

*although there is a chance of reperfusion arrhythmia it does not indicate reperfusion.

7. The patient is admitted with acute pulmonary edema. The pO2 is 48, pCO2 is 57, the blood pressure is 160/90, pulse 122, respiratory rate is 36. The most appropriate initial intervention:

a. bi-level positive airway pressure (BiPAP)

b. Continuous positive airway pressure (CPAP)

c. Pressure control ventilation

d. Inverse ratio ventilation

*Lots of experience on telemetry with this for those CHFers and Acute on Chronic COPDers. We just have to remember that for BiPAP the patient must be able to maintain own airway and that the duration is for less than 48 hours. Usually that is enough time anyway to turn things around with some Lasix and Dig. 🙂

8. The pathologic changes found on a 12 lead EKG to indicate myocardial ischemia are:

a. ST elevation

b. ST segment depression and T wave elevation

c. Q wave formation

d. ST segment depression and T wave inversion

* ST elevation shows injury. Q wave formation indicates necrosis. The keyword is ischemia for this question.

9. Failure to capture is a complication of pacemakers that might be caused by:

a. Lead maturation

b. Lead displacement

c. Dead battery

d. Open circuit

* Failure to capture is the pacer is firing and you see the spike, but there is no qrs following it. Open circuit is a broken lead wire. Lead maturation is normal.

10. Automatic implantable cardio-defibrillators-AICDs- might be initiated in the treatment of:

a. Frequent PVCs

b. Atrial fibrillation

c. Narrow complex SVT

d. Symptomatic VT

*Those at risk for sudden cardiac death, cardiomyopathy.

Hopefully I did not bore the internet with this, but who wants to study alone? Not me!

Apparently these are the easy questions. It has to get harder, right?


Lazy

25 Jun

OK I have been a lazy nurse blogger.

I should study for the PCCN exam! Yaay! (not) It is so hard to get back to test prep.

Anyhow…..Here goes a test question– an easier one on the pretest

1.  A patient with admitted with heart failure is on a diuretic and fluid restriction. Assessment indicates atrial tachycardia with a rate of 130, presence of crackles in all lung fields,  an S3 heart sound at the left apex and a blood pressure of 90/40 (previously 130/60). The patient reports feeling short of breath. The nurse should anticipate the administration of………….

(mulitple choice question–pick 1)

A.  a fluid bolus to enhance preload

B. dopamine to support the blood pressure

C. dobutamine to augment cardiac output

D. adenosine to reverse the tachycardia

wOOt! who knows the answer?!? (answer below)

 

 

 

 

 

 

 

 

 

 

 

C. dobutamine!!!!

PCCN

18 Jun

I am studying to take the PCCN exam in approximately 2 months! I did the pretest to see how I will stand up without studying first. I did great on the cardio but terrible on everything else!! Imagine that? The ABG analysis killed me! The endless questions about urine osmolarity perplexed me!! Mostly because the questions were not is this ,or is this not normal, but rather, “What is the expected intervention?”

Just when you think you are super duper cool nurse, you find out the impossibility of knowing it all.

I guess I will just have to take only patients who are: Acute MI, NSTEMI, CHF, A Fib,  Acute Pulmonary Edema, Pulmonary Embolism and Sepsis!!!!!             

Is that all I have learned so far?

Studying will commence immediately.

I feel so special.

Oh and if you do not know what the PCCN exam is click here on PCCN.

Oh and Nurse K has a sadly amusing post about admissions and bed shortage and telemetry beds: click here. And read about the shell game. It is true to the word. A few weeks ago I started the shift with 6 patients: Sent 2 to the medical floor, 2 to rehab, and 1 went home. Guess how many admissions? Ironically the 2 that went to rehab and the1 that went home were long gone before the medical floor would take report on the other 2 ! I am not sure how it is possible that every time I call to give report they are, in an isolation room, or having lunch!?! I can only imagine the wrath if I did not take report from the emergency dept on a patient immediately ! We just do not do that on my floor, the sooner I get the patient the better for me and the patient and the hospital.