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It’s An Automatic.

6 Jan

Drawing from http://xkcd.com/175/

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Fast Atrial Fibrillation

3 Aug

It is Atrial Fibrillation with a rapid ventricular response. The atrial rate can be more than 300 beats per minute followed by the ventricular rate of up to 170 beats. That is fast. I like to say in my mind Fast AFib. It just sounds cooler.

The intravenous cardizem is infusing giving a better control, or not.What about the or nots? I bet EPS Dr Wes, could give us the facts.

Why does it always have to be intravenous  cardizem?  I have seen Multaq post cardioversion sustain a nice sinus bradycardia. I have a love/hate relationship with Amiodarone.

I am a fan of the digoxin added to a beta-blocker.  I am starting to dig digoxin more and more because it does not drop the blood pressure.

 

Falling

28 Apr

Credit: me_falling_down_by_HiroPonLover

Oh credit the artist. deviantART has the best artists on display. Check them out.

That is me falling down. I like the pink hair and the socks.

I fall down inside of myself. Dx: Emotional Syncope. The belly starts swirling and the chest gets heavy. I should wear a falls risk bracelet.

I work in a small hospital, on a telemetry floor. I have not figured out who gets admitted to the medical floors yet.

My favorite Cardiologist likes to write STOP TELEMETRY orders with letters so big the two words take the space of half of the page.

 

I am happy with my small heart.

20 Apr

skAte Love by DoT Dep

credit the devianARTist. Yeap. I have been crushing on devianART for years, there are some fine artists over there.

That skate board is busted. It will never fly again. Some hearts get broken, never to beat again. Sometimes they can be fixed. Sometimes you just want someone to crack your chest open, while you are awake, show you that you do have a heart and then kiss it with an antibiotic lip.

Alcoholic induced cardiomyopathy can get better with the cessation of alcohol and some beta blockers, they say. Stress induced cardiomyopathy, ya know, the broken-hearted syndrome? It is totally reversible, do not let anyone fool you. Next time you get upset and you feel it in your heart: just tell yourself this: This is nothing more than catecholamines being released tearing me up, and basically stunning my heart.

So, I do not need a big heart. I do not want dilated ventricles and hypertrophy and the cycle of that reckless compensatory mechanism that all starts with the low cardiac output sans dehydration.

I am happy with my small heart. ❤

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

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.