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14 Apr

Cartwheel by bobbipop

credit the artist on deviantART by clicking on the picture.

I like to do cartwheels. I do them all the time. Anywhere, anytime I feel like my heart needs it. On the grass, or on the black top, I am that 4 pointed object wheeling around the lot. Cartwheels are better in the grass. I like to take my shoes off when I do them so I can point my feet to the sky. Seriously, it is all about the heart. I bet when I do cartwheels it increases the venous return to my heart, and that makes me feel good.

I mock trend on my bed all the time too, but cartwheels are way more fun.

I want to go do cartwheels and round-offs right now, but I have to make sure that I know what it is that I do at work every week, and why I do it. I guess that is what certification is. I am already doing this, I already learned it, so I should just pass the test with pretty colors.

There is only 5 questions on the Endocrine system, and they will be about DKA and hypoglycemia.

Here is what I will remember!

When a DKA patient goes pee pee they will dump glucose and electrolytes out and that includes potassium. Insulin drives potassium into the cells. So the patient needs insulin and electrolyte replacement.

Hypoglycemia yikes. Half the time, hospitalized patients are not eating! Feed the patient. We do not have to run and push D50 all the time. That amp of D50 is caustic to the veins, if the patient is awake just feed them!

Hematology and Immunology have 3 questions, that is 2%.

Here is what I will remember!

The rule of 3s cake.

The RBCs x 3=the hemoglobin

The hemoglobin x3= the hematocrit.

If the Hb times 3 is less than the hematocrit the patient is dehydrated.

If the Hb times 3 is greater than the hematocrit there is fluid overload.

Platelets. Bleeding for nothing can happen with platelets less than 25.

For sure I am not inserting a rectal tube into a patient with super low platelets.

Gastrointestinal has 6 questions that is 5% of the exam. Yuck.

GI has lots of information for only 6 questions. Do you remember from nursing school that for acute pancreatitis, Dilaudid is the drug of choice for pain relief because Morphine may cause biliary colic or spasms of the sphincter of Oddi? Yeap, start laughing but I got that question right in nursing school.

There is Ranson’s Criteria to determine mortality and acuity. Acute pancreatitis patients just look sick, and they are sick. Imagine an organ eating itself.

Remember for the test that: Grey Turner’s sign bruising blue around the flank and that Cullen’s sign is around the umbilicus.

The GI hemorrhage, well it really smells bad and that is all I have to say about that. Most of these bleeds are caused by peptic ulcer disease, and next in line is the esophageal varices. Actually, I wonder why coumadin therapy is not on the top of this list, because certainly I care for lots of anemia for the coumadin patient!

Hepatic Failure, is ugly. The yellow, poopy, lactulose, change of mental status climbing out of the bed mess is just awful. The ascites, hypotension and tachycardia is nerve wrecking.

Yeah I am bored now, if you are bored too, well that makes this less painful for me somehow, sorry. I am not going to kill myself writing about portal hypertension, or the lovely memories of that first GI bleeder.  After this is over, I will write some poetry to make up for this pain.

Here are some practice questions. I am not going to write the multiple choice answers because well, I am out of time for that trickery.

1. What is the peak of rapid acting insulin?

60-90 minutes

2. A new diabetic should be closely monitored when taking which cardiac medication?

beta-blockers *can lower blood sugar

3. Treatment of metabolic acidosis from DKA consists of

a.insulin administration

b. bicarbonate

c. low salt diet

d. fluid volume resuscitation

* you can not mask the acidosis with HCO3

4. The patient has a blood glucose of 400, with lethargy and deep gasping resps. The ABG is pH 7.28, CO2 30, HCO3 14 (partially compensated metabolic acidosis) is most likely from:

diabetic ketoacidosis

5.Symptoms of thrombocytopenia include:


6. Ocreotide is often used to control bleeding from esophageal varices, the primary action of this drug is to:

decrease the blood flow.

*it also decreases gastric secretions.

7. An elderly patient is with severe abdominal pain. What should always be ruled out?

bowel infarction

8. Pulmonary complications from acute pancreatitis may include:

ARDS and elevation of the diaphragm and bilateral rales and atelectasis, especially in the left base.

9. Which lab finding is most specific for pancreatitis?

elevated serum and urinary amylase

10. I am not doing this anymore.

Tomorrow I will blast through the neurological section. I already know I have a whacked out limbic system, but I love it. I mean I love my limbic system.

I will go do cartwheels now.


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.


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.


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!


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!

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
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.

Don’t lose heart

10 Apr

Take my Heart by F_AYN_T

Credit the deviantARTist by clicking on the art.

She thinks she does not want her heart right now, but believe me, she will change her mind when the heart starts screaming for oxygen. You know,  when there are ECG changes, high troponin and chest pain, we will all want our heart back.

I am moving out of the cardiovascular system, even though I would like to circulate here for a while. I won’t lose heart, I am going to pulmonary next which is my next favorite thing, and the second largest content portion on the exam.

Before I go: here are the antidotes to reverse the following:

methemoglobinemia give methylene blue

organophosphates like pesticides give atropine

acetaminophen give acetylcystine

opiates give narcan

And be careful reversing benzos with ramazicon, please.

Not related to the heart but surely on the exam. I doubt I will be studying much during the next 3 days, I am working my 3 in a row.

I will keep my heart, now give me some LOVaphed please.

You are dynamic

8 Apr


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


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


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


*well surely not tPA!

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

Ten more

6 Apr

Credit the artist: Heart by ~snul found on deviantART.

That is some cardiomegaly she is carrying around. It reminds me of cardiac remodeling. It must be heavy carrying around a large heart. It just does not function properly. The whole stretch, Starling thing.

Don’t tell me I have a big heart! No thanks, I am happy with my skinny heart. ❤

I really wish someone would distract me, to prevent me from being sucked in to the bodies compensatory mechanism during heart failure that actually exacerbate the failing heart.

The thing is, when the heart is failing, and cardiac output is decreased the body does not know why cardiac output is low. The body actually thinks the person is roaming through the desert, dehydrated with no oasis in sight, so it activates the SNS, the RAAS, and the aldosterone system to: increase the heart rate, vasoconstrict and hold on to salt and water. When the pump is failing these are the things we do not want to happen, so we give drugs, like beta-blockers  and diuretics to stop the bodies natural compensation and prevent more work for the heart. I mean seriously, the failing heart can not pump out the blood it has, and therefore these systems just make everything so much worse.

If only the failing heart could say: Yo! I don’t need your compensation, just let me rest! You are making me work harder!

It can’t so we give drugs.

10 PCCN questions with some rationales, the same as before. Answers are underlined and colored red for cardio LOVE again.

1. You hear an S4 gallop during assessment, this may signify:

a. Heart Failure

b. Decreased compliance of ischemic myocardium

c. Aortic stenosis

d. Increased left ventricular filling volume

*The atria contract and blood is forced into and non compliant ventricle, it is a stiff wall and the sound is heard before S1

2. Heart failure caused by the inability of the heart to fully relax is:

a. Systolic

b. Diastolic

c. BiVentricular

d. Complete

* the heart can not relax, the forward flow is decreased and the EF is normal in diastolic heart failure as opposed to systolic failure the contraction is weak. The treatment right now appears to be the same.

3. The primary function of drug therapy with beta blockers in heart failure is:

a. Increase blood pressure

b. Block compensatory mechanisms

c. Increase urine output

d. Decrease arrhythmias

*See the opening speech on this post.

4. Early symptoms of fluid overload and pulmonary edema:

a. Rales and hypoxia

b. S3 and tachycardia

c. Increased respiratory rate and subjective dyspnea

d. ST segment elevation in the chest leads

*The earliest symptoms are increased resp rate and shortness of breath. When the fluid moves into the interstitial space, the lungs are still clear and the patient seems anxious.

5. Which coronary artery supplies the atrioventricular node?

a. Right coronary

b. Coronary sinus

c. Left anterior descending

d. Nodal artery

*The right coronary artery supplies the right side of the heart and the bottom of the heart, the electrical system is in the right side of the heart.

6. The S4 heart sound occurs:

a. After ventricular contraction

b. Is best heart with the diaphragm of the stethoscope

c. Is a normal finding in children

d. During atrial contraction

*Again S4 is heard when blood is pushed into a noncompliant ventricle and this happens during atrial contraction.

7. A 20 year old athlete collapsed playing sports and was resuscitated on site. He is awake and orientated now but having many PVCs. What is the most likely reason for this cardiac arrest?

a. Myocardial infarction

b. Pericarditis

c. Peripheral vascular disease

d. Cardiomyopathy

*Changes in the structure of the heart.

8. The patient has palpitations, the tele monitor shows sinus tachycardia. What is the initial treatment?

a. Adenosine

b. Defibrillation

c. Treat fever, pain or dehydration

d. Valsalva maneuver

*NOT a STAT cardio consult and check the hemoglobin.

9. An inferior wall myocardial infarction will show changes in what EKG leads?

a. V1 to V4

b. V1 and AVL

c. V5 and V6


*I have a hard time imagining the 12 lead to heart anatomy so I just memorize.

10. The most common complication of an acute myocardial infarction:

a. Dysrhythmia

b. Congestive heart failure

c. Cardiogenic shock

d. Pulmonary embolism

*While cardiogenic shock is the worst case scenario, the most common complication is dysrhythmias, they might be having PVCs.

Pretty straight forward so far, nice forward flow. The only problem is that I want to be distracted, so I will either play words with friends, if someone will entertain me, or I will go on to read about: what is going on with diastolic versus systolic heart failure treatment and the future of that, or I will go play outside since the sun is popping out.

Test date April 21. I still have a lot to study and I am wasting my time apparently studying cardiac, the stuff I already know.