Tag Archives: CHF

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.

Why does it shrink?

12 Apr


Look at these cozies for urinal bottles. Give me a break!    Who in their right minds would come up with this crap. Ewwww…Germs. yucky.  The label says they are FDA approved and machine washable. Yeah right! We can barely get clean linens and chuck pads never mind the worry over who is going to wash and  supply urine bottle sleeves for what, patient comfort? Ewww…

RN + 80 year old male CHF patient on  massive doses of IV Lasix.

During morning assessment finds 80 year old male CHF on massive doses of IV  Lasix, at the edge of the bed, fumbling with the urinal, peeing all over the floor, looking perplexed and fondling his penis.

Looking at the pee on the floor and the nervous man.

RN-What is going on in here? (getting gloves and towels and pulling the curtain closed for privacy all at the same time)

Patient–Why does it always shrink in the morning?

RN–ummm…I am not sure about that. hmmmmmm…

RN to Cardio MD (later that day) umm…the 80 year old patient on massive doses of IV Lasix in CHF with strict intake and output monitoring needs a catheter. It apparently shrinks in the morning and pees all over the floor, so if you want the output measured in patient peed on the floor, just let me know.

Strict I and O

8 Mar

I just do not understand how Dr Cardiology can write in the same chart on the same patient everyday–“Strict I and O please and document”

What does Dr Cardiology not understand when Nurse tells him that the patient is incontinent especially while coughing? (A river comes out)

We all understand that medicare will not pay for hospital acquired urinary tract infections but this is ridiculous! If you want strict output for very good reasons ie: The patient is on a lasixgtt then please give us, the nurses the green light to insert the catheter! How else will you know if the plan is working? By daily weights alone? Give us a break! Be brave young cardiologist you know the patient needs it.

I mean how is it possible to have a patient, on lasix IV and dobutamine IV in severe uncompensated CHF and not have a foley catheter in, urinating all over the bed half in the bottle half on the chux pad? The output will be documented in number of pads, not volume of urine.

And yet 450 pound chronic pain patient who refuses physical therapy has foley catheter in for days and days and days and days and days. (?) No sense. How did that patient even get a foley cath inserted?

I must have missed a point somewhere. errr.