Day 9: Cardiac Labs, Cardiac Diseases, ECGs, Hemodynamic Monitoring, Shock

Cardiac Labs

(...with some deviation into kidneys and liver, cause it's all related.)

(Okay, but seriously, I haven't looked at this in 9 months.
This is going to be a beast of a post.  Bear with me.  Haha, get it?)

Here are the lab values I (you) need to know for cardiac diseases:

Serum electrolytes (in order of greatest numerical range to least, just to make sure I remembered what I relearned yesterday) 

• Na+ 135-145
• Cl- 95-108
• Ca2+ 9-10.5
• K+ 3.5-5
• PO4^3- 3.5-4.5
• Mg2+ 1.3-2.1

ESR: 1-13 (the Mayo Clinic says 1-22**)

C-reactive protein: risk for CAD  normal <1; average 1-3; high risk >3

PTT: 16-40; aPTT 1.5-2.5X norm

PT/INR: 11-12.5/0.7-1.8 (2-3 on coumadin)

BUN: 10-20          Video on BUN here

Creatinine: 0.6-1.2    

LFTs:

• Cholesterol <200
• Triglycerides <150
• LDL <130
• HDL <65
• Albumin   3.5-5
• AST aspartate aminotransferase and ALT alanine aminotransferase 0-35 (signs of hepatitis)
  Video on liver function tests here
• ALP alkaline phosphatase 30-120 (biliary tree obstruction)

BNP: no failure <100, possible failure <300, failure >300 (300 mild, 600 moderate, 900 severe)

Creatinine phosphokinase MB (CK-MB): <5% (<25 IU/L)

Troponin: <0.2***

*I didn't remember any of them (yikes), so I looked them up in my ATI book.  And yeah, I know all of these values are without units, but the NCLEX is not going to try some bitchy unit swap on your to make you fail, and they aren't going to ask you to convert cholesterol units. 

** Also, if the values look different, then, well... don't worry that much about it.  The likelihood you'll pull the question on the value you don't know is slim, and when you work in the real world, each institution has their own "normal range."

***There's 2 troponins, but my guess is that T is the one used more often because it has the same early detection time (3 hours), but it lasts for longer (21 days vs 10).  The other one is Troponin I and it lasts for 10 days and <0.03 is normal.

ECGS

I confess, aside from there being 6 seconds a strip and knowing the general shape of a PQRST I've totally forgotten how to read these.  So, let's figure this out together, shall we?

Basics:  Strips on the test will come in 6 second sections.  Each itty, bitty square is 0.04 seconds of time (you don't have to memorize this).  And usually, the strips come with bold(er) lines that outline groups of 5 "0.04 second" sections in 0.2 second sections, like this:

So each "thick gray box" is actually 0.2 seconds x 0.5mV, which matters because:

PR interval should be between 0.12-0.2 seconds (3-5 tiny boxes)

QRS complex should be <0.12 seconds (3 tiny boxes)

You don't really need to get a whole lot more specific than that, except for a few points (like hypokalemia has a flat or inverted T because the threshold for firing has been lowered--but you don't have to memorize numbers for that).

https://s-media-cache-ak0.pinimg.com/originals/77/9e/c3/779ec32d585f55813ecfd7c8b07f7acf.gif

The questions you should ask yourself when you look at an ECG are:

1) Is it regular?

2) What is the rate?  

• If it's not regular, count the QRSs and multiply by 10 (6 seconds x 10=1 minute).
• If it's regular, I prefer the: 1500/ # of small boxes between two consecutive R-R intervals*

3) Are P-waves present?

4) If the P-wave is present, is the P-R interval normal (0.12-0.2 seconds=3-5 blocks)? 

5) Is the QRS normal (<0.12 seconds=3 blocks or less)?

* Why 1500?  Because there are 1500 tiny boxes in 1 minute of EKG strip.  Prove it?

5 tiny boxes x 30 gray boxes x 10 "6 second strips"= 1500 tiny boxes in 1 minute of EKG strips

So, a normal sinus rhythm:

http://nuclearcardiologyseminars.com/wp-content/uploads/2013/11/nsr.jpg

1. Regular (meaning, the number of boxes between each R peak is the same-ish): In this case, about 21 boxes between each peak.
2. The rate is between 60-100 (remember: 1500/# of small boxes between two consecutive R-R intervals):1500/21=71bpm
3. You see a distinct P-wave: Yup, little bump right before the QRS.
4. And the P-R interval is between 0.12-0.2 seconds (3-5 blocks): almost perfectly 3 each time.
5. And the QRS is tall, and less than or equal to 0.12 (3 blocks) long: almost perfectly 3 each time, also.

Here's a rundown of common dysrrhythmias.

Sinus bradycardia:

1. regular
2. rate 1500/# r-r interval boxes <60
3. P wave present
4. P-R interval 3-5 blocks
5. QRS tall, less or equal to 3 blocks

Causes: IICP, hypoglycemia, hypothermia, Valsalva, medications (B-blockers, dig, Ca2+ channel blockers), but it can also be a natural reaction to be really athletic or sleeping, so it's only treated with atropine, dopamine, epinerphine, pacemakers, and the existing medications that are slowing the heartrate should be reduced or discontinued if the patient is symptomatic.

Sinus tachycardia:

1. regular
2. rate 1500/# r-r interval boxes >100
3. P wave present
4. P-R interval 3-5 blocks
5. QRS tall, less or equal to 3 blocks

Causes: physiologic/psychological stress such as dehydration or hemorrhage, angina or general pain, fever, etc., and stimulants, or stimulant drugs like epinephrine, norepinerphine, atropine, caffeine, theophylline, hydralazine, and pseudoephedrine.  Treatment: Treat the stressor, vagal maneuvers, B-blockers, adenosine, Ca2+channel blockers, synchronized cardioversion.**

Premature atrial contraction:

1. irregular
2. rate 1500/#r-r interval boxes 60-100
3. P wave "looks funny," eg biphasic (squiggly looking)
4. P-R interval 3-5 blocks
5. QRS tall, less or equal to 3 blocks.

Causes: Stress or fatigue, hypoxia, electrolyte imbalances, hyperthyroidism, COPD, heart disease, valvular disease, or use of caffeine, tobacco, or alcohol.  This may indicate a reentry mechanism that may become SVT, or enhanced atrial automaticity.  Treatment: Beta blockers and cessation of sympathemimetic drugs.  

Atrial flutter:

rate: varies

rhythm: regular atrial flutters up to 350 bpm accompanied by slower ventricular regular or irregular rhythms
P-waves are sharp and irregular, giving a "saw toothed" appearance.
P-R interval not measurable because of multiple P-waves.
QRS usually normal.

Causes: Almost always some cardiac disease (CAD, HTN, mitral valve, PE), cor pulmonale, hyperthyroidism, dig, quinidine, epi, which will cause decreased cardiac output and clotting.  Treatment: Blood thinners (heparin, then warfarin, slow ventricular contractions if needed with Ca2+ Beta blockers, and electrical cardioversion if unstable, otherwise antidysrhythmics (ibutilidem, amiodarone), and radiofrequency catheter ablation.

A-fib:

Rate & Rhythm irregular, very tiny atrial oscillations that are completely unmeasurable (I don't care what your books says, you're not going to be able to count 600 oscillations).  Ventricular contractions irregular
P "fibs"
unmeasurable P-R
QRS usually normal.

Causes: multifocal ectopi due to underlying cardiac disease (even pericarditis, and also surgery), tyrotoxicosis, ETOH, caffeine, electrolyte disturbances.  Treatment: the priority is to decrease HR *if* the ventricular response is "uncontrolled" or "rapid" (>100) with B-blockers, Ca2+ blockers, dig.  Otherwise, if the patient is symptomatic (losing consciousness) cardioversion ONLY IF the patient has be in a-fib for less than 48 hours and/or a transesophageal echocardiogram rules out clots in the atria.  If they have been fibbing for more than 48 hours, they have to be on 4 weeks of warfarin (INR: 2-3) before you cardiovert or you could dislodge a clot and kill him or her.  Non-cardioversion antidysrhythmic options are amiodarone and ibutilide.

Junctional Dysrhythmias: When the SA node fails and the AV node becomes the pacemaker, and the impulse moves backwards, producing a P wave occurring before, after, or under the QRS complex.  P waves appear to be premature atrial contractions.  

• Junctional bradycardia = junctional rhythm at a rate of < 40 bpm.
• Junctional escape rhythm = junctional rhythm at a rate of 40-60 bpm.
• Accelerated junctional rhythm = junctional rhythm at 60-100 bpm.
• Junctional tachycardia = junctional rhythm at > 100 bpm. 

Rate: regular
Rhythm: often bradycardia (the AV node beats 40-60), but if some SA node impulses occur, it can be higher when the sympathetic stimulation  to improve CO.
P waves vary, but often are "invisible" as they are covered by the QRS, and sometimes inverted
P-R interval varies
QRS usually normal

Causes: cardiac diseases, digoxin, nicotine, amphetamines, caffeine.  

Tx: atropine for bradycardic rhythms, B-blocks/Ca2+/amiodarone for tachycardic rhythms.

The AV blocks:

1st degree AV block--Normal rate and rhythm for A&V, normal P, P-R>0.2 seconds, normal QRS

2nd degree AV block--Normal and regular A, slower V, multiple P:V ratio, P-R cannot be calculated since there are multiple P waves, widened QRS.  Progresses to complete heart block due to His-Purkinje disease.

3rd degree AV block--P appears abnormal because some will be hidden under QRS--this is because it is complete heart block and the pacemaker that is able to set the ventricular rate is the AV node=severe bradycardia,  multiple P:V ratio, P-R cannot be calculated since there are multiple P waves, wide but consistent.   Hemodynamically very unstable.

Causes: medication (B-block, Ca2+, dig) or cardiac damage/valve disorders.  1st degree has no real treatment except to discontinue medications if the block is medication related, 2nd and 3rd degree are treated with atropine, amiodarone, and pacemakers.

Paroxysmal supraventricular tachycardia: technically any ectopic anywhere above the birfucation of the Bundle of His, usually triggered by an extra pathway that bypasses the AV node causing a reentrant phenomenon (like with Wolff-Parkinson-White syndrome, which is a type of atrioventricular reentrant tachycardia, which is a type of supraventricular tachycardia--yeah, I know, confusing.  You'll get it eventually).  

rate: regular

rhythm: Tachy

P-wave: oftentimes obscured

P-R interval: varies if present at all

QRS: usually normal

Causes: overexertion, stress, deep inspiration, stimulants.  But also from dig, CAD/rheumatic heart disease, cor pulmonale.  Treatment vagal stimulation, adenosine, amiodarone, B-block, Ca2+ block, if hemodynamically unstable, synchronized cardioversion, and radiocatheter ablation.

Premature ventricular contraction: comes from ectopic foci in the ventricles.  If the QRSs originate from different foci, each QRS will look different and that is called "multifocal PVCs."  If they originate from the same foci, the QRSs will look the same and that is called "unifocal PVCs."   Sometimes you have normal sinus, then a PVC--bigeminy.

Sometimes you have 2 normal sinus, then a PVC--trigeminy.

Sometimes you have normal sinus, then two PVCs in a row, then normal sinus--couplet (of PVCs).

If you have 3+ PVCs, that's considered ventricular tachycardia.

rate: anything

rhythm: can be regular, can be irregular, can even be regularly irregular

P-wave: usually hidden under the QRS

P-R: nonexistant (duh ^^)

QRS: wide and distorted

Causes: stimulants, amniophylline, epi, dig, electrolyte imbalance, hypoxia, fever, stress.  Treatment: remove stressor--if hypoxic, give oxygen, if fever, give tylenol, if stress, reduce stress, if stimulants, excrete stimulants, etc.  Give B-block, Ca2+ block, procanimaide, amiodarone.

Ventricular tachycardia: 3+ PVC's.  One type of V-tach is Torsades de Points, which is a polymorphic VT and a prolonged QT interval.  V-tach can quickly degenerate into V-fib.

rate: 250+

rhythm: regular

P-wave: invisible

P-R: nonexistant (duh^^)

QRS: varies

Causes: Prolongued QT (sometimes caused, ironically, by antiarrhythmics), genetics, heart damage (MI/CAD), CNS disorders/electrolyte imbalance.  

Treatment: If pt has a pulse: procainamide, sotolol, amiodarone, implantable cardioverter-defibrillator

If a patient does not have a pulse: CPR, D-fib.  If d-fib unsuccessful, follow with vasopressors (epinephrine), antidysrhythmics (amiodarone).

Ventricular fibrillation: tiny squiggly line.  NO PULSE.  CPR, D-fib.  If d-fib unsuccessful, follow with vasopressors (epinephrine), antidysrhythmics (amiodarone).

Pulseless Electrical Activity:  PEA is where you see electrical activity on the screen, but there is no pulse in the patient.  It is most commonly seen after D-fib (for v-fib or hemodynamically unstable v-tach), and the only thing you can do for this patient is CPR and try to figure out what is causing the PEA.  Causes include: The H's and the T's (see below)

• hypovolemia (give volume, obviously: PRBCs, D5W or .9NS wide open, elevate the legs, do whatever you need to do to make the systemic volume go up--remember pressors only work if there is adequate volume in the body already)
• hypoxia (O2, really sucks if it's carbon monoxide poisoning...)
• met. acidosis (bicarb, regular insulin with D20W, potassium if the etiol is hypokalemia--highly unlikely, I know--and intubate that person because you better believe his ventilatory drive is in the toilet with respiratory fatigue from trying to blow off CO2.)--Yeah, I  know this is neither an H or a T.  Whatever.  It was in my textbook.
• hypokalemia (give potassium IV DILUTED)
• hypoglycemia (D20W)
• hypothermia (warm .9NS)
• toxins (antidotes, dialysis, chelation)
• cardiac tamponade (decompress the pericardium--no, not you, the doctor)
• thrombosis (suck that sucker out--not you, the doctor)
• tension penumo (insert chest tube)
• trauma (fix it, whatever it is)

Sudden Cardiac Death: if I remember correctly, usually happens to young people who were just really active sending them into Vtach or V-fib, and you just need to do CPR and D-fib until help arrives with epinephrine and amiodarone.

Prodysrhythmia: this is when antidysrhythmic medication like dig, or amiodarone causes the same dysrhythmias for which they were prescribed.  Yup.  It happens.  I don't know how to treat it directly--that is the doctor's job to figure out.  I just treat according to what the EKG looks like until the doctor figures it out.

Asystole: CPR, treat the cause.  Epinerphine, vasopressin.    Causes include: hypoxia, acidosis, electrolyte imbalance, drugs, hypovolemia, cardiac tamponade, tension pneumo, MI, hypothermia, trauma.

But basically, I hope you started to see a pattern here:  Any time there's an inconsistent rhythm you were given an antiarrhythmic like amiodarone or ibutilidem.  Any time the heart was going too slowly, there was atropine.  Any time the heart was going too fast, there was B-blocks, Ca2+ channel blocks, dig.  Any time the patient was hemodynamically unstable but still had a pulse, cardioversion.  Once there was loss of consciousness but still electrical signal, CPR, then d-fib, epi, and amiodarone--except with PEA, where you have to figure out all the hypos or to toxins, thrombosis, tension pneumo, or trauma.  

ECG PRACTICE HERE

CARDIOVASCULAR SYSTEM DISORDERS

btw, Khan Academy (which you should all donate to), has free tutorials and NCLEX-RN questions on this cardiac dysrhythmias.

Quick repost of lab values:

ESR: 1-13 (the Mayo Clinic says 1-22**)

C-reactive protein: risk for CAD  normal <1; average 1-3; high risk >3

PTT: 16-40; aPTT 1.5-2.5X norm

PT/INR: 11-12.5/0.7-1.8 (2-3 on coumadin)

BUN: 10-20          Video on BUN here

Creatinine: 0.6-1.2    

LFTs:

• Cholesterol <200
• Triglycerides <150
• LDL <130
• HDL <65
• Albumin: 3.5-5   
• AST aspartate aminotransferase and ALT alanine aminotransferase 0-35 (signs of hepatitis)
  Video on liver function tests here
• ALP alkaline phosphatase 30-120 (biliary tree obstruction)

BNP: no failure <100, possible failure <300, failure >300 (300 mild, 600 moderate, 900 severe)

Creatinine phosphokinase MB (CK-MB): <5% (<25 IU/L)

Troponin: <0.2

Here are a few ECG variations you should remember for Acute Coronary Syndrome:

MedSurg by Lewis Dirksen Heitkemper Bucher 9th edition, page 806.

Note, how ischemia (reversible) will result in an ST-segment depression >1box in at least 2 leads, and possible T wave inversion; injury will result in ST-segment elevation; infarction (cell death) causes BOTH the ST-segment elevation, and the T-wave inversion.  Often times if a patient is not showing signs of an acute attack, yet the ECG shows signs of ST-segment elevation or T-wave inversion, you can tell that they had a heart attack in the past.  This is pertinent with cardiovascular disorders.

Hypertension:  Ok, so hypertension can occur because of multiple reasons (pheocromocytoma, renal failure, heart failure, bad diet, and the race most affected is African Americans, especially the men) but whatever the case may be, in the end you need to do the same basic things: eat a heart healthy diet (low sodium, low fat), exercise.  If your hypertension is bad and has caused damage to your kidneys, AND/OR your hypertension is now worsening because your kidneys have conked out on you (remember, you can tell that a person is in renal failure if the creatinine>0.6-1.2; and especially if both Creat:BUN are elevated but the ratio is still 1:10 to 1:20, so like Creat 20:BUN 300.), you need to offload that fluid before you drown (pulmonary edema) with ACE-inhibitors and diuretics, and you need to help your poor, beat up heart (Ca2+ blockers, B-blocks, dig) beat better.

I'll do a review of these medications in another post.

Angina: comes in 3 forms:
1) stable (triggered only by exertion and stress)
2) unstable (fatty deposits rupture/blood clots form, suddenly blocking a narrow artery=suddden decrease in blood flow) that is not relieved by medications
3) variant aka Prinzmetal, very rare, and is a spasm in the coronary artery.

Risks are (of course) family history, smoking, hyperlipidemia (cholesterol>200; Triglyc>150, LDL>130, HDL>65), which often accompanies sedentary lifestyle and obesity, and diabetes.

If a patient presents to the ER in acute onset of angina (s/s of acute coronary syndrome), assess the patient for location of pain, character of pain, duration of pain and whether it was relieved with rest or nitro on scene, and what precipitated the onset of angina (and of course eliminate those triggers to avoid addition attacks while in the ER).  

then, administer MONA in this order:
1) Oxygen (ABC)
2) Nitro
3) Aspirin
4) Morphine
and then, 5) thrombolytics.

and, if necessary, prepare for transport to the cath lab or surgery.  If the patient is stabilized and the doctor feels that it is unnecessary to do PCI, then anticipate beta blockers, aspirin, nitrates, statins, Ca2+ channel blockers, and angiotensin converting, enzymes.

In the real world, you may give MONA immediately without getting an ECG, because the sooner oxygen and blood flow is restore, the more likely you are to recover from ischemia and not progress to injury or infarction, but for the purposes of the NCLEX, you always assess first--it is NCLEX world in perfect harmony, and the patient will not die before you finish your assessment.

Cardiac catheterization: There are two types of cardiac cath for ACS: coronary angioplasty (a balloon is inflated at the site of blockage and mashes the fat against the wall to create a bigger opening), and coronary stent (the same thing as an angioplasty, but you leave behind a fine mesh to keep the fat from collapsing in as soon as you back out of there).

The main things you need to remember as a nurse for cardiac cath is: it's percutaneous (percutaneous coronary intervention), may require dye (check for shellfish allergy--although, many of my doctors have said that the correlation between shellfish allergy and dye allergy is a debunked myth, so who knows), so you will need to:

• NPO
• verify consent
• shave prep (always a trick question whether to shave or to cut hair at the site with scissors to microcuts and prevent infection.  I've never known sources to agree--it's like, whatever, you're going to use betadine/chlorhexadine in a second, who gives a fuck.)
• explain dye--"you may feel flush and taste a metallic tang," and check for allergies
• mark baseline pulse

Your main concern is hemorrhage through the femoral artery (and it has to be the artery because you're going into the coronary arteries and that's the only way to them--it's not like you can go through the ICV and thread through the alveoli and back out into the aorta), so:

• APPLY PRESSURE FOR 15 FULL MINUTES (at least, especially if PT>12.5/INR>2-3), oftentimes you'll use a sand bag to maintain pressure, and KEEP THE LEG EXTENDED--in fact NO HIP FLEXION IN BED for 4-6 hrs.
• monitor hemorrhage q 15 min for the first 4 hrs, then 30 minutes, then hourly, etc.
• monitor neurovascular q 15 min for the first 2 hours, then 30 minutes, etc.
• increase fluids (for hypovolemia, and to wash out dye)

Anticipate the doctor will put the patient on the same medications as for a patient with stable angina without PCI, that is: beta blockers, aspirin, nitrates, statins, Ca2+ channel blockers, and angiotensin converting, enzymes.  You'll have to teach the patient to avoid the valsalva maneuver, avoid stress/sudden bouts of physical activity (ESPECIALLY in the cold--Jesus.  All of those people who suddenly decide that they're going to shovel their house out of a blizzard and end up dying of heart attacks on their sidewalk), rest after eating (especially hard to digest things, like steak), and stop smoking.  Exercise LIGHTLY--seriously, walking is enough--and eat a heart healthy diet.  (Like, duh.)

So, with the medications you have to teach:

nitro--SIT YOUR ASS DOWN, take with onset of angina SL q 5 minutes up to 3 times.  Call 911 if it's not relieved after the first tablet.  Keep the nitro in a dark, dry container out of the light and away from heat, and replace q 6 months even if you've never used it--don't be cheap about this medication.  If you're taking it and you don't get a headache, maybe the nitro isn't working.  If you're taking nitro on a daily basis (as a cream or a patch) you have to use it for ONLY 12 hours a day (applying it in the morning) and wash it off for the other 12 hours to prevent developing a tolerance.  And do not take it if you are on a sildenafil (Viagra) because your blood pressure will bottom out and you will die.  I mean, be nicer than that, but make sure that the patient gets that this is serious.

Ok, so you've had angina, and a cardiac cath, and you're still eating McDonalds, or you haven't given up your job as a top litigator and then you decided to go shovel your house out in the middle of a blizzard and you've had a full on grade A heart attack and given yourself a massive myocardial infarction.  Maybe you went into V-fib, had to be D-fibbed and had someone pound on your chest and break a few ribs the whole way from your house in the back of an ambulance to the hospital, where they discovered that a piece of artherosclerotic gunk broke off in spite of the coronary stent, and got lodged in your left coronary artery.  They cracked you open, did a CABG on you, and now you're in ICU, in extreme pain (fun fact: diabetics, due to diabetic neuropathy, may not report pain), and your ECG is showing simultaneous ST-segment elevations and T wave inversion.  (Which reminds me, I really have got to exercise today...)

Myocardial infarction:  s/s: severe chest pain (or not, with diabetes, women or elder patients) unrelieved with nitro or rest that crushes and radiates to jaw, left arm, neck, back, etc.  Diaphoresis, N/V anxiety, ECG shows tachycardia/dysrhythmias c possible ST elevation (STEMI) and/or T inversion, hypotension + dyspnea.  Expect troponin>0.2, CK-MB>3,  LDH (lactic acid dehydrogenase) >140-200, 

Nursing goal: Rest the myocardium and preserve heart muscle.

MONA: 

Immediately: Oxygen, nitro, aspirin, morphine, streptokinase or alteplase (within 6 hours), amiodarone, calcium channel blockers.

Later: stool softeners + bedside commode, promote self care and exercise but stop if fatigued or angina occurs, heart healthy diet, stress management, smoking cessation.

Discharge medication: heparin, aspirin, warfarin, enoxaparin, clopidogrel (antiplatelet), metoprolo, diltiazem (Ca2+), nitro, simvastatin (antilipidemia).

The result of a myocardial infarction is heart failure.

Heart failure:  A chronic condition where the heart is unable to meet the body's oxygen requirements, and is often accompanied by fluid overload/inadequate tissue perfusion + fluid retention due to decreased renal circulation.  Depending on what caused the heart failure (cor pulmonale, which coronary artery was blocked, kidney failure, hypertension, etc.) there may be L.S. HF (symptoms are related to decreased systemic/pulmonary circulation, i.e. elevated PAWP, pulomonary edema and paroxysmal nocturnal dyspnea, low O2 sat), or R.S. HF (symptoms related to systemic congestion, i.e.  acites, hepatosplenomegaly, dependent edema + fluid weight gain, elevated CVP, JVD, anorexia/vomiting)

Ok, wait, but what is the PAWP and the CVP?  I ask, because I know it has to do with catheters measuring pulmonary artery wedge pressure (PAWP) and central venous pressure (CVP), but that's about all I remember.  So, let's take a side trip into HEMODYNAMIC MONITORING.  If you already got the theory, here's the hemodynamic values you should know:

CVP: 1-8mmHg
PAWP: 4-12 mmHg
Cardiac output 4-8L/min = Stroke volume x Heart Rate
Mean arterial pressure 70-105 mmHg = [systolic + 2diastolic]/ 3
Systemic vascular resistance 1970-2390 gynes/sec/cm^-5= [(MAP-CVP) x 80]/ CO
Arterial hemoglobin saturation 95-100%
Mixed venous hemoglobin (SCVO2): 60-80%

If you didn't take the side trip, basically, you need to know that elevated levels of CVP (>8)and PAWP (>12) mean that the heart is (for whatever reason) unable to pump blood efficiently.  In the case of heart failure, it's because of heart failure (duh).

Treatment of heart failure= pump it, park it, pee it=focuses on decreasing fluid volume overload and helping the heart to pump more efficiently (inotropic medications)/decreasing systemic vascular resistance.  

Medication for inotropic (pump it): digoxin

Medications for decreasing systemic vascular resistance (park it): B-block, Ca2+ ch. block, nitrates/hydralazine, nesiritide, milrinone, dobutamine.

Medications for decreasing fluid (pee it): ACE inhib, ARB, diuretics

Coronary artery bypass graft (CABG): usually requires an open chest surgery with bypass (ECMO).  Your job as a nurse is to:

preoperatively: VS, assessment, HX.  support (psych and anxiolytics), teach the family and patient to anticipate intubation, IV lines, foley, arterial line, chest drainage tubes.

postoperatively: hourly assessement for first 8 hours of complications:

• vitals, neurological (pupils, reflexes, Glasgow)
• cardiac: CVP, PAWP, ECG, sounds, increased bruising, etc., peripherals
• resp: ventilator settings
• renal: I&O, electrolytes, urine specific gravity
• pain: location, type, intensity, onset

DVT: usually caused by increase in thrombi formation (think estrogen in pregnancy or contraceptives, or long term immobility from injury, immobility, or age).  You'll see a red, hot swelling of one limb, that may be bumpy, knotty, and shiny (edema leaking through).  You may see a venous ulcer (usually medial side of the leg at the ankle or above).  It is best prevented by ambulation, weight loss, wearing supportive antiembolitic socks, and elevating the lower extremities and not crossing your legs, and preventative SQ heparin.  It is diagnosed with an MRI, Spiral CT, U/S, and then treated with heparin (PTT 60-100) and warfarin (INR 2-3), alteplase, elevating the extremity, applying warm, moist compress, and being vigilant for s/s of PE, stroke, or MI.  Otherwise, sclerotherapy, ligation and stripping, or thermal ablation may be necessary.  

Peripheral artery (occlusive) disease (PAD): Peripheral arterial disease is just a buildup and consequential narrowing of arteries.  It is a significant risk for future major coronary events--note the name "peripheral artery disease" is misleading because atherosclerosis can happen all over the body, such as in the heart (CAD) or in the brain (cerebrovascular disease).  As such, the risk factors of PAD is the same as those for CAD, which are, high cholsterol >200, high triglycerides >150, and elevated CRP >3, smoking, diabetes, etc.  S/s include: intermittent peripheral claudication pain that resolves with rest (because decreased blood flow will exacerbate the removal of lactic acid), and calf muscle atrophy, and shiny skin with hair loss, paresthesia, and thick toenails (signs of decreased oxygen and nutrients reaching cells), and may lead to leg ulcers.

Leg ulcers are another thing that I found really confusing because it's never really well explained.  I'm still not good at it, but as I've said before, I've accepted that there are many things that will make sense to me, and that I will learn after I've passed the NCLEX.  To see a quick differentiation of leg ulcers, take a look here.  

Along the same vein, there is a similar disease called...
Thromboangiitis obliterans aka "Buerger's disease": a disease that causes repeated inflammation of the blood vessels of the extremities, resulting in idiopathic thrombosis and occlusion.  This also has the symptom of intermittent claudication, inflammation due to clots, and cold skin that is relieved by rest, smoking cessation, avoiding caffeine, and avoiding constrictive clothing or the cold.  If it is prolonged open sores may occur on the fingers and toes that require amputation.

To make things more confusing, there is another similar disease (that actually popped up on my NCLEX-PN as the final question) called...
Raynaud's syndrome: a disease that causes vasospasms/constriction of the arteries due to exposure to cold and stress.  These may lead to ulcerations of the fingertip, so the patient should wear extra clothes in the cold, but make sure that the clothes are not restrictive.  Smoking cessation, and limiting caffeine intake is also suggested.  You could also administer nifedipine.  Nifedipine would NOT work with thromboangiitis obliterans because there is inflammation and thrombosis involved.

Structural Cardiac Disorders

Valvular disorders: valve disorders are mostly cases of stenosis which makes it difficult for the heart to eject blood, but also, allows for backflow (leaking) back into the chamber that was just pumping.  Just remember the side each valve is located (R: tricuspid, R pulmonary, AV; L: mitral, aortic, AV).  Murmurs are just the turbulence of blood sloshing around erratically because of the stenosis or prolapse.  Mostly it leads to heart failure.  The only treatment is surgery for replacement, which will require warfarin for life if it's mechanical, and immune suppressants if biological (but warfarin only for 3 months).  If you have an autologous fancy, valve, you won't need either except in the immediate postoperative.  All of the valve surgeries will require prophylactic antibiotics for any further procedure to prevent infective endocarditis.  

Aortic aneurysm: usually caused by congenital connective tissue disorders, but also from infection and atherosclerosis.  An aortic aneurysm greater than 5 cm requires surgical intervention.  Usually a patient doesn't even know he has an aortic aneurysm.  He may complain of:

• thoracic pain, dyspnea, hoarseness, cough, and dysphagia (remember, the larynx, pharynx, esophagus, trachea, are all in the mediastinum with the aorta and the heart)
• lower aneurysms (remember, the abdominal aorta is still part of the aorta) may cause abdominal pain, persistent or intermittent low back or flank pain, and you might actually be able to see a pulsating abdominal mass

Your job as the nurse is to: 

Preoperative: maintain systolic between 100-120 with beta-blockers, antihypertensives.  Continuous nipride might be prescribed, and to be vigilant for signs of rupture (sudden, intense pain with rapid BP drop).  Also, you'll have to care for the patient during CT scans, MRIs, X-ray, and ultrasound.

Postoperative--basically the same as preoperative because now, instead of an aneurysm, you've got a line of sutures holding the aorta together.  Freaking hell!  And of course, infection.

SHOCK

Ah, shock.  So many versions.  So confusing.  I'd encourage you to make a chart in the end to get an overview, but I'm just going to talk about each separately.  I personally found this Khan Academy video very helpful.  There is also a collection of review questions from Khan Academy.  As I said before, I highly suggest donating to them since they provide excellent education for free, which helps those who come from socioeconomic hardship to have the same education someone of means might get from a private school.  Here's a great story showing that.  

First off, shock is any situation where there is decreased tissue perfusion and impaired cellular metabolism, resulting in cell starvation.  There are 4 main categories: cardiogenic, obstructive, hypovolemic, and distributive.  

Cardiogenic shock, obstructive shock, and hypovolemic shock are the ones you'll most see on TV. They're slightly difficult to tell apart because they all have some form of decreased cardiac output, and in response the blood vessels constrict in attempt to increase blood return to the heart.  In addition, all three have decreased mix oxygen content (MVO2) because the body's cells are desperately trying to pull as much oxygen out as possible, resulting in a low oxygen content in the blood returning to the heart.  They deviate when it comes to preload levels.  In cardiogenic and obstructive shock, you'll see an increased PAWP>12 (remember, this measures how much pressure is in the ventricles at the end of diastole) because the ventricles are unable to properly eject blood out of the heart either because the heart is damaged (like from an MI) and unable to pump (cardiogenic shock), or because there's an obstruction (like an aortic stenosis or cardiac tamponade) preventing the blood from flowing (obstructive shock).  In hypovolemic shock, there simply isn't enough volume in the body to properly fill the ventricles (because of dehydration or hemorrhage) resulting in a lower PAWP<4.  With cardiogenic shock you have to fix whatever damage there is to reestablish proper circulation, and with obstructive shock you have to either unplug the thrombosis or open the stenosis.  With hypovolemic shock you have to fix the source of the bleed, or simply refill the body with blood components and/or fluid.  The emergent steps to stabilize a patient (for surgery): 1) Establish airway, give O2, and 2) improve circulation and contractility with epinerphine (vasopressor) and IVF, and 3) then repairing the problem.  

Distributive shock: Neurogenic, septic, and anaphylactic

Neurogenic shock, which occurs when the spine is injured, causing an impairment in sympathetic response.  Neurogenic shock is the only shock that results in a BRADYCARDIA and simultaneous decrease in nervous system tone (blood vessel dilation).  So, the spine is injured, HR drops, causing cardiac output to decrease (SV x HR= CO<4L/min), and the blood vessels aren't constricting.  PAWP isn't really affected even though there is decreased vascular resistance. Mixed oxygen saturation should be low because the blood is traveling slower so the surrounding tissue has more time to absorb O2.  Treatment should be to maintain BP: pressors, IVF, atropine (blocks the parasympathetic nervous system=stops rest and relax signals to increase the heartrate).  

___________Detour into neuro for a second:  SCI

With SCI, if the injury is above T6, there is a risk of autonomic dysreflexia should the patient experience bowel impaction, bladder distension, triggering of pressure points, ulcers, or pain.  Autonomic dysreflexia is a life-threatening syndrome of sudden, extreme hypertension, with bradycardia (30-40bpm).  Other s/s: H/A, piloerection, flushing above the level of the injury, blurry vision, nasal congestion, and nausea.

The order of nursing actions is:

• High fowlers (I know, your first instinct is to roll that person over and try to un-impaction him, but, don't, cause that may not be the problem.  Putting the person in high fowlers buys you time to assess the causation)
• (have someone else) alert the physician
• determine and remove causative stimuli--also remove anything that may cause more stimuli to the patient
• give medications (lidocaine, to help with digital fecal removal and/or bladder cathing, a-blockers, and Ca2+ channel blockers)
• teach bowel and bladder management

________________________End detour

Septic shock and anaphylactic shock are another couple that have strong similarities.  Septic shock and anaphylactic shock both have immune mediated systemic vasodilation, which causes edema (resulting in decreased circulating volume, and makes it more difficult for O2 to diffuse from the blood vessels to the tissues). In both, PAWP is marginally decreased, but not by much, if at all.  The treatment for septic shock is 1) (Airway, Breathing) ventilation; 2) (circulation) IVF, pressors, 3) treat the source with blood cultures and ABX (desire CRP<1, ESR <20-25 = decreased inflammation, and decrease bacterial count), and the treatment for anaphylactic shock is 1) establish airway with ventilation, 2) maintain BP with epinephrine (and open airway) and IVF, and 3) continue to reverse the allergic reaction with benadryl.

There's also something called dissociative shock in which hemoglobin doesn't release O2.  There are 2 causes of dissociative shock.  The first is: sometimes a person has red blood cells where the iron in the hemoglobin is Fe3+ instead of Fe2+.  Fe3+ (ferric ion=methemoglobinemia) causes Fe2+ hemes to increase in ferrous ion oxygen binding.  This is caused by nitrates, especially antibiotics, (such as TMP/SMX, and dapsone), or anesthetic (like benzocaine), or pesticides.  Neonates are especially vulnerable to methemoglobinemia because they're missing an enzyme that converts Fe3+ to Fe2+.  Treatment of methemoglobinemia is IV methylene blue, which causes Fe3+ to be converted back to Fe2+.  The other cause of dissociative shock is CO (carbon monoxide) poisoning which has a 100X greater binding ability to hemoglobin than O2.  It causes a change in shape of the hemoglobin, preventing their release.  The cause of CO is carbon combustion, like a fire burning stove.  Treatment is oversaturation with O2 in a barometric chamber.

Day 13-12: Nursing Care of Children--Newborn and Infant Standard Tests, Complications and Congenital Anomalies

Oh, newborns.  So exciting and cute.  So freaking complicated and scary.  I mean, all of nursing is complicated and scary, but babies, especially.  Because they're small.  And fragile.  And weird.  Their circulation is weird, and their breathing is weird, their vital signs are weird.  They're wet.  And slippery.  And floppy.  And you have to poke and prod and test their Moro reflex, which makes them cry, and you just about lose your shit because evolution has wired us to want to give babies whatever they want to make them stop crying.  

Before we get into APGARS (yay, more to memorize...)

Newborn VS:

HR: <100 if sleeping, 110-160, up to 180 when crying.  Protip: I find tapping my finger while counting their tiny apical pulses for a full minute helpful with babies because otherwise I lose count.

Respirations: 40-60, usually shallow and irregular.  There is transient apnea, but the apnea should never be more than 20 seconds.  Look for nasal flaring, intercostal/supra/subcostal retractions, or see-saw breathing.  

Temperature: 99.7-98.9F axillary.  Temperature instability is a sign of infection.

BP: 60-80/40-50.  Hypotension=sepsis/hypovolemia; Hypertension coarctation of aorta.  

So, you delivered the head, cleared the mouth, then the nose (the mouth first to prevent aspiration), delivered the rest of the body, cut the cord, now what?

Apgar was named after the person who invented it (Virginia Apgar), yes, but more importantly, APGAR stands for:

A: Appearance completely blue (0); acrocyanosis (1); completely pink (2)

P: Pulse zero (0); <100 (1); >100 (2)

G:Grimace (with stimulation) no response (0); grimace (1); crying (2)

A: Activity (is the baby flexed) limp (0); some flexion (1); well flexed (2)

R: Respiration: zero (0), weak/<40 (1); good cry/>40 (2)

The numbers you need to remember with APGAR are: 4 and 8.  4 (repeat 4, 4, 4, 4, 4, 4) and up is moderately distressed (3 and down is severely distressed), 8 and up is WNL.  APGARS are taken at 1 minute and 5 minutes after birth, and only again at 10 minutes if the child does not improve/is still below 7 at 5 minutes.  Note, the stimulation for grimace is just drying the baby and getting him warm.  

For APGAR practice click here.

Once that is complete, the baby is printed and secured with an identity band for mom, dad (or mom mom or dad dad or whatever), and baby.  And as long as baby is stable, we can begin feeding immediately after birth, and every 2-3 hours after with breastfeeding, and 3-4 hours with formula (formula digests slower, and you have to burp them ever 1/2 ounce or 1 ounce, and you have to chuck it after 1 hour of being prepared to prevent bacterial contamination).  Here is proper latch on positioning, note the football position for C-section moms.  We want a minimum of 100mL/kg in the first 24 hours.  So, for example a 6 pound baby would be 2.7 kg x 100 mL/kg=270 mL.

[FYI: 16 ounces/1lb

so,  if the baby is 6lbs 7 ounces 

that's 6pounds + (7ounces/16ounces in a pound)= 6pounds+ 0.43pounds=6.43 pounds

--> convert to kilos

6.43pounds/2.2pounds per kilo=2.9kilos

--> multiply that times 100 mL/kg in the first 24 hours

=290 mL

but if they give you a problem, then the creator of that question is an asshole.

But you might have to calculate that in real life.]

GU: the baby needs to pee within the first 24 hours of life, and after the 4th day of life, urination occurs 6-10 times a day.  They usually poop within 48 hours.  Poop usually looks yellow and seedy. Teach that circumcised penises can be cleaned with warm water, and to apply petroleum jelly with each diaper change (q 4 hours minimum), and that yellow mucus is ok and to leave it on.  It should heal in 2 weeks.  Don't submerge the kid in a bath until then, cause the umbilical cord has to dry and fall off first (and you just clean that with a neutral pH cleanser and sterile water at birth, but otherwise it should remain dry until it falls off).  

For reflexes go here.

For the Ballard Score go here.  I'm not going to memorize that because I don't have time for that.

Standard care and labs for newborns include:

1. eye prophylaxis with erythromycin (for GCCT--aka gonorrhea and chlamydia) within the first hour of birth
2. vit K IM injection within the first hour of birth
3. Hep B within the first 12 hours.  
4. ABO Rh type and screen
5. PKU
6. CBC:

• RBC 4.8-7.1 million
• Hgb 14-24, Hct 44-64
• WBC 9-30,000
• platelets 150,000-300,000
• glucose 40-60  (within 2 hours of birth)**
• bilirubin day 1: 0-6; day 2: <8; day 3 <12;  hyperbilirubinemia >15 at any time 

Any time a baby is stressed (from withdrawal, from cold, from illness, from RDS) it will burn more calories.  It is important to check glucose (hypoglycemia=2 consecutive <40 in term, <25 in preterm--remember preterm is before 36 6/7 weeks).  Babies with hypoglycemia are jittery, cold and clammy, and eventually become flaccid and/or have seizures and slip into a coma--AND IT HAPPENS QUICKLY.

Transitional Periods

After the baby is born, it has 3 transitional periods: 1) first period of reactivity=first 30 minutes of life, which is the best time to breastfeed, 2) sleep from 30 minutes to 2 hours old, 3) second period of reactivity from 2 hours till 8 hours, where gagging and vomiting usually occurs, and then they feed again.  (Awww, so cute.)

Guthrie test:

http://www.homebirth.net.au/wp-content/uploads/2010/02/new+born+screening-450x237.jpg

Phenylketonuria

Every baby is tested for phenylketonuria 2 days after birth by federal mandate, with the Guthrie test (heel stick) which is a genetic condition where the baby cannot break down phenylalanine from protein into tyrosine.  The infant starts off with failure to thrive, vomiting, irritability, hyperactive/erratic behavior and ends up with brain damage (older children display schizoid behavior like catatonia, screaming, biting, and head banging).  Treatment means a protein restricted diet with no sweetners for life, and the baby must have a special phenylalanine-free formula (like Phenex-1).  

Substance Dependent Babies

Fetal ETOH syndrome: Since ETOH is a depressant, the lack of a depressant will result in an irritable baby, crying, seizures.  Other problems are IUGR, smaller/thinner/flatter than normal craniofacial features, and possible deafness.

Nicotine: premature, low birthweight, increased COPD (bronchitis, pneumonia), developmental delays, and increased risk of SIDS.

Opioid: sneezing, poor temperature regulation, hyperactive Moro reflex, CNS irritability-->seizures (especially with methadone).

Cocaine: shrill cry, tremors, sleeplessness, muscles spasms, feeding problems.

Often phenobarbital is prescribed for seizures.  Decrease stimuli, swaddle, small frequent feedings of high calorie formula (possibly gavage).  Many struggle with poor sucking of they can settle down enough to eat at all, so preterm nipples with larger holes are used, but try to breastfeed because it has been found to help ease withdrawal symptoms (the drugs carry over, especially if mom is on methadone to help kick the habit).  

Premature Babies (<38 wks)

Premature babies have a low birth weight, little fat (brown fat deposits insufficient, which increases impact of cold stress or oxygen deprivation stress so cluster care and keep the baby warm), long periods of apnea (10-15 seconds), and may not be able to suck/gag/swallow/cough (before 34 weeks) so will require parenteral nutrition.  Also, the child may suffer from RDS.

Respiratory Distress Syndrome

Occurs with premies, babies with meconium aspiration (aka perinatal asphyxia or stress asphyxia), and with C-section babies because they haven't had enough surfactant produced (premies), or they have fluid in their lungs (part of the compression of the torso required to pass through the pelvis squeezes out the fluid from the lungs and helps the baby draw its first breath).  Oftentimes they will have intercostal or substernal retractions, nasal flaring, grunting, rales, cyanosis, etc.  So, administer beractant (a synthetic surfactant), and don't suction for 1 hour so it can spread across the inside of the lungs.

Post-term Babies (>42weeks)

Post-term babies are at risk for injury during delivery (shoulder dysotcia, fx clavical, brachial plexus injury, or facial paralysis), possible risk of degenerating placenta causing meconium aspiration, hypoglycemia, and jaundice.  Initiate early feeding, and watch for signs of pneumonia or jaundice.

Hyperbilirubinemia 

(Bilirubin >15)

There are two types of jaundice: physiologic ("natural" or "expected") and pathological (has a disease process).  Physiological jaundice occurs gradually (>24 hours later), and is caused by the natural breakdown of extra RBCs from mom.  Also, it can happen because newborns have immature livers (less clotting factors), and there is a lack of Vit K.  Pathological is jaundice that sets in within 24 hours of birth and/or lasts more than 7 days, and has an increase in bilirubin at 5mg or more a day, and is caused by blood incompatibility between the mother and the child, or from an infection, which can lead to kernicterus (brain damage due to bilirubin >25).  Direct Coombs to test for sensitized RBCs.  Treat with phototherapy (break q4hr to unmask eyes and check for inflammation or injury)--keep the kid naked, except for the genitals, and protect from burns (no oils or lotions), dehydration (lots of water), and hyperthermia.  Feed the baby frequently to excrete bilirubin in stools (will look loose and green).  If the baby is at risk for kernicterus (bilirubin >25), you may have to give an exchange transfusion.  Kernicterus starts with the same stress symptoms as any other disease (lethargy, poor feeding, temperature instability, and hypotonia-->progresses to fever, seizures, and high pitched cry, and will result in cerebral palsy, mental retardation, upward gaze paresis, and hearing loss.

An easy way to remember risk factors for hyperbilirubinemia in full term infants is the acronym 

Jaundice <24 hrs after birth (physiological)

A sibling who was jaundiced as a neonate

Unrecognized hemolysis (incompatibility--remember, Rhogam @28 weeks and at birth or any trauma), or delayed cord clamping=increased blood volume

Nonoptimal sucking (slow GI=re-unconjugation of bili in the intestine goes back into the bloodstream)

Deficiency in glucose-6-phosphate dehydrogenase

Infection

Cephalohematomas/bruising during delivery

East Asian or Mediterranean descent

CONGENITAL ANOMALIES: CARDIAC

http://cardiovascularsystemud.weebly.com/uploads/8/2/1/2/8212050/5709166.jpg?822

Quick A&P review, basically the fetus gets oxygenated blood from mom (the umbilical vein--remember vein means blood returning to the *fetal* heart) via the ductus venosus (vein, get it?), where it mixes with the deoxygenized blood from the fetus' own vena cavas.  The fetal heart circulation bypasses the lungs (shunts a little to help the lungs develop, but for the most part nothing goes to the lungs), by 1) flowing through the foramen ovale (a hole between the atriums) to be ejected by the left ventricle into the aorta, and 2) being shunted from the pulmonary artery through the ductus arteriosus (artery, get it?) into the aorta.  Once the baby is born, the foramen ovale and the ductus arteriosus should close, and the lungs open, and the baby gets its own 100% super oxygenated blood in through the left side of the heart just like we adults do.  All circulatory congenital defects have a breakdown in that transition.

Almost all require surgical intervention except maybe PDA or ASD.  These can be fixed with indomethacin which closes the holes.  If left unfixed they all result in poor growth and development, and some degree of heart failure, and some of them (like TGV) result in death.  Atrioventricular septal defects will result in a systolic murmur.

PDA

http://www.drugs.com/mcd/images/image_popup/DS00631_IM01560_r7_patentductusthu_jpg.jpg

PDA--the ductus arteriosus doesn't close.  Most of the time it is asymptomatic, but sometimes there is a heart murmur and a wide pulse pressure because the aorta is getting a fuckload of blood from both ventricles, resulting in a high systolic.  The left ventricle has to work super hard.  Treatment: indomethacin and/or surgery.

Atrial Septal Defect (Patent Foramen Ovale)--The foramen ovale didn't close.  The blood is bypassing the lungs.   Treatment is surgery during preschool years (3-6 y-o).

Ventricular Septal Defect--Really large defects are called "Eisenmenger's complex."  You'll hear a big systolic murmur, and heart failure.  Small defects close spontaneously, large ones require surgery during preschool years.

http://www.drugs.com/mcd/images/image_popup/DS00615_DS00998_IM00438_r7_tetralogythu_jpg.jpg

Tetrology of Fallot--1) Pulmonary stenosis, 2) VSD, 3) overriding aorta, 4) R. ventricle hypertrophy.  This kid is seriously sick, and gets acute cyanosis and hypoxia called "tet" spells.  Squatting helps to increase systemic vascular resistance, reversing the shunting and getting blood to the lungs and helping to oxygenated the blood.  If this is hard to understand, put your finger over the aortic arch and imagine no blood can flow out that way (this is what happens with systemic vascular resistance).  Now the blood has no where else to go when the ventricles pump *but* to the lungs.  This kid usually has clubbing of the fingers and severe growth retardation.  Surgery is necessary within the first few years of life.

TGV with ASD

http://static.bandbacktogether.com/media/images/2012/02/tgvdiagram.jpg

Transposition of Great Vessels--This is the condition I personally call "I don't know how this baby survives 3 minutes after birth," because the aorta is connected to the right side of the heart, and the pulmonary artery is connected to the left side of the heart.  The only way this baby survives is if it ALSO has VSD, ASD, or PDA, or SOMETHING that allows it to somehow circulate oxygenated blood between the two sides.  It's insane.  The treatment is to continue giving prostaglandins to keep the ductus arteriosus open and surgery is immediately done to swap the aorta and pulmonary artery back into the right place.  It's absolutely insane.

https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgDG40D8hE0ANywVcGt_I8LIpM_Oym-ChVDMRGpz7w2j7A36g2mUG_AcIluUzO0LcIHAFNCKbOgn0rqvKy0SzyprrPlc9k2FphMqKT7Z9vYPexFx0xZvBZ32nfP7q3T1-zmx4PE-3WD6jLV/s1600/Postductal+coarctation+of+the+aorta.png

Coarctation of aorta--So basically the aorta is narrowed, and the lower extremities don't get enough oxygen or nutrition.  The left ventricle has to work extra hard to fight past that narrowing, causing heart failure.  However, look at what those three little arteries at the top of the aortic arch flow to:

https://www.netterimages.com/images/vpv/000/000/013/13922-0550x0475.jpg

Increased blood pressure to the carotids can cause hypertension with headaches, epistaxis, and intraventricular hemorrhage--remember the infant's blood pressure is only 60-80/40-50 because those little brain blood vessels are very fragile.


The nursing considerations for children with these congenital heart defects are: cluster care, provide small, frequent, high calorie meals with plenty of time to eat (gavage if necessary), avoid making the babies cry (I don't know how to not make a baby cry with gavage...).  Observe for infection since these kids are at higher risk.  Give medications to decrease the labor on the heart--like digoxin (0.5-0.8) hold if AP <90 (this is different than adults where the threshold is 60), Ca2+ channel blockers like captopril or enalapril, and duretics like furosemid or chlorothizide.  

CONGENITAL ANOMALIES: SKELTAL

Clubfoot--To call clubfoot a purely congenital anomaly is a lie.  The truth is we have no idea what causes it.  Probably some sliding scale of genetics to intrauterine positioning.  Club foot has 5 different manifestations you need to be concerned with:

http://odlarmed.com/wp-content/uploads/2009/04/talipes_clubfoot.jpg

1) talipes equinovarus--the most common, with plantar flexion and feed bending midline.  To help you remember the name, equin/o/varus means "the heel elevated like a horse" (hence "equine") and "turned inward" (hence "varus").

http://www.nursing-help.com/wp-content/uploads/2011/08/image60.png

2) talipes calcaneus--the heel down and the toes up as if in permanent dorsiflexion.
3) talipes equinus--again, with the heel elevated like a horse.

http://www.nursing-help.com/wp-content/uploads/2011/08/image59.png

4) talipes varus--as before, the toes turning midline
5) talipes valgus--the toes turning laterally

Whatever the cause, it is identified either with ultrasound or at birth. with radiography done to see the extent of the deformity.  After the child is born, massage for lesser degree malformation can be used to manually straighten the foot/feet, or serial casting (changing the cast q2 weeks for 12 weeks) until maximum correction is achieved, and then application of a (rather medieval looking) Denis Browne splint or reverse last corrective shoes to maintain the correction.  If the correction is too late, or not effective enough, surgery with ORIF may be required between 3-12 months of age.

Danis Browne splint:

https://upload.wikimedia.org/wikipedia/commons/8/83/Botas.JPG

Hip Dysplasia: hip dysplasia, in its most basic form, is when the femoral head and the acetabulum are unstable or dislocated. This can happen with acetabular dysplasia (the abnormal development in utero), a complete dislocation (during breech birth, or LGA, or late-term babies), or subluxation (a partial dislocation)--keep in mind even those that are due to "injury during birth" may also have some genetic predisposition. (Also, remember that during the pregnancy, the mother is releasing progesterone, and progesterone makes everything squishy, including the baby's ligaments.  And the baby itself is cartilaginous.)  This is why after the baby is born we do a physical where one of the jobs is to flip the baby over and look for symmetry of their gluteal and thigh fat folds.  And we hold them upright to see if one knee hangs lower than the other (remember when something is dislocated, the muscles suck the bones past each other so the dislocation actually looks shorter), which is called the "Allis sign."  We also use Barlow (intentionally testing if the femoral head can be dislocated) and Ortolani's (if dislocated, then reducing the dislocation) test.

https://www.youtube.com/watch?v=imhI6PLtGLc

Yeah.  I know.  Scary as fuck.

The treatment for hip dysplasia is a Pavlik harness that prevents hip extension or ADduction for infants <6 mos, and Bryant's traction and surgery to reduce with infants >6mos (or the Pavlik harness didn't work) with the addition of a hip spica cast.

So the basic care of both hip spicas and long leg casts (in the case of genu varum/valgus, or clubfoot), is ABC (checks q15) and by not applying the cast too tightly or smushing it while its drying, infection/skin care from pressure sores, etc. (you can apply "petals" of padding with tape around the edges of the plaster--especially around the window where urine and defecation take place), and also pain and psychosocial distractions for the baby, and nutritional needs (constipation from reduced movement).  The parent may also need special strollers or car seats.


CONGENITAL ANOMALIES: NEUROLOGICAL

***Remember that AFP, or MSAFP is something you *screen* for in the first trimester with an integrated first trimester screen along with Tri21 and Tri18, and in the second trimester with quad and penta screens.  Normal AFP is <2.5 MoM for singlets.

Neural tube defects--There are three main levels of neural tube defects you need to be concerned with: occulta, which is where everything is still sealed, meningocele, which is where the meninges is still intact and there's just a little bubble protruding out of the back, and myelomeningocele or "spina bifida," which is when there is an open spinal defect and the meninges (remember the meninges are the three layers of spinal membrane covering the nerves that encase the spine and the brain into one sac) are open and the spinal fluid and nerves are all spilling out.

Complications are hydrocephalus, clubfoot, scoliosis, congenital hip dysplasia, bowel and bladder problems...

Treatment is prevention (all women of child bearing years should take folic acid supplements since the spine fuses by week 10 and often times people don't know they are pregnant until after 10 weeks). After the child is born the treatment is surgery.

The nurse's job presurgery is to preserve the integrity of the meninges by keeping the infant prone and covering the protrusion with sterile saline moistened gauze.  You don't cover the sac with clothes or diapers, and you have to be careful to clean the perineal area well to prevent tears or cracks in the meninges or the development of meningitis.  Note that children with NTDs have an increased risk for latex allergy.  Postsurgery, keep the infant in prone, monitor for IICP and hydrocephalus.  If the child's injury causes bladder and bowel nerve damage, teach the parents CRede's maneuver and the child how to self-catheterize around age 5-6.  Oftentimes the patient won't be able to feel if she has a UTI, so it's important to teach monitoring for infection (foul smell, cloudy urine, temperature).

Hydrocephalus-the imbalance of absorption of production of CSF inside of the cranial cavity, and/or the obstruction of the flow of CSF through the ventricular system.  Sometimes, hydrocephalus develops later in life due to a malformation such as a neoplasm, infection, or trauma.

The infant will have increased head circumference with bulging anterior fontanels and distended scalp veins.  They will be irritable, have a high pitched scream, and it is extremely uncomfortable for them to be cradled horizontally.  Children with hydrocephalus like to be held upright--this relieves pressure from their cranium.  An older child may verbalize headaches, blurry vision or diplopia, vomiting in the morning, and even experience seizures.

This kid needs seizures precautions both pre and post-op for realz, and constant neurological checks (like we said before, for children, it is measuring thee circumference of their occiptal frontal region).  After the surgery you position the baby on the non-shunt/non-surgery side (you can use a wedge to keep them tilted up on one side), and watch their VS. like a hawk.  Watch for sudden changes in consciousness, vomiting, and sudden increase in difficulty with feeding.  Also, for infection--cause, you know, meningitis is bad.  Also, teach the family TO WASH THEIR DAMN HANDS when handling the kid especially when pumping the shunt to relieve CSF pressure.

Cerebral Palsy-at it's most basic qualification, cerebral palsy is abnormal muscle tone and lack of coordination with spasticity (often with contractions) either of diplegia (both legs), hemiplegia (one side of the body), or quadriplegia (all 4 limbs).  These children often have delayed milestone development and have a lot of back arching and dystonia or ataxia, but little other spontaneous movement including sucking and swallowing (so feeding can be challenging).  Often these children have intellectual, visual, hearing, speech and language deficits, and can have seizures.  Most cases of cerebral palsy are due to brain insult, whether in utero, during delivery, or after birth (such as sepsis or hyperbilirubinemia or PKU, infections like with meningitis/encephalitis like with spina bifida, toxins, or stroke).  Obviously we stop whatever is the offending situation (give mom O2/side lie/stop the pit/emergency C/S, treat infection with antibiotics, give an exchange transfusion, etc.), but after birth, you just treat the symptoms (seizure medication, OT, PT, speech therapy and modify the environment)

Yeah.  Scary as fuck.  You still with me?

Okay.

CONGENITAL DISORDERS: GASTROINTESTINAL

The first two are easy to differentiate: Hypertrophic pyloric stenosis and Cleft lip/palate
Hypertrophic pyloric stenosis- is a thickening of the pyloric sphincter that may show up as an olive-sized mass in the upper right quadrant of the abdomen.  Failure to thrive, projectile vomiting, and constant hunger are positive signs, plus an U/S to confirm.  The child will have to undergo surgery and have an NG tube and be NPO until bs returns.  Things to teach the parents include: side lie with head elevated when vomiting, watch for dehydration, assess the incision for infection, and otherwise hold the kid and give pain medication when the child seems to be indiscomfort.

Cleft-lip/palate--The test question material that always gets me with cleft-lip/palate is to maintain nutritional intake with a soft, elongated, or premie nipple, or with mom breast feeding because it fills in the cleft.  A last resort would be NG tube or parenteral feeding.  The baby should be fed in an upright position with frequent burping to prevent eustachian tube infection and extra gas.  And the baby should be fed no less than four hours before surgery.  After surgery, the suture integrity needs to be maintained with cleansing with normal saline or sterile water and sterile technique (seriously?  it's the inside of the mouth...ok)  and a cotton swab, or half strength peroxide if a crust has formed.  Feed with an Asepto syringe or dropper to the side of the mouth, and suction gently and lay the baby on its back, but preferably on its side to maintain airway patency and avoid rubbing the stitches.  Antibiotics and pain medication.

See?  Stitches.  Laying the baby on its face is a stupid idea.

http://67.199.56.100/adam/dochtml/graphics/images/en/7057.jpg

Here's where the confusion occurs:

NTD is PRONE.  Cleft-lip is SUPINE or SIDE.

Kind of duh, but I panic and mix them up on the test all the time. 

Maybe I'm just stupid.

The next two are more similar: Hirschsprung's (which should just be called "congenital aganglionic megacolon," because "Hirschsprung" doesn't help a person remember a single thing about this disease) and Intussusception.

Hirschsprung's- Basically, part of the large intestines doesn't have nerves (aganglionic), so it doesn't have peristalsis.  Think about a moving walkway in an airport.  Say you throw a whole bunch of baggage on the moving walkway, but that section of regular floor between two moving walkways doesn't move, so the baggage piles up at the end of the moving walkway part, and then everything gets backed up.  That's Hirschsprung's.  Fluids will flow around the blockage, so you'll get diarrhea, but otherwise things back up so much the kid ends up projectile vomiting.  There's a lot of pain, too, and peristalsis waves that are visible to the naked eye (cause the kid will be skinny from malnutrition), and worn down enamel from throwing up constantly.  Treatment is: serial rectal irrigation to decompress the bowel, then surgery to resect the aganglionic section, then possibly a colostomy and NG-tube/NPO for a bit until the intestines recover.  And antibiotics and pain medication.

Intussusception:

http://giphy.com/gifs/animated-illustration-motion-study-XhxVN2AQxB4LC

Intussusception- Imagine the intestines fold on each other like a captain's spyglass being collapsed.  It happens most often at the ileocecal valve and is accompanied by sudden and with acute pain with "currant jelly stools" of blood and mucus.  You diagnose with a barium enema (which may actually straighten things out by pushing the ileum back out of the colon).  And you treat with air injections or barium enemas.  If that doesn't work then you cut that section out.  Also you give PPI's (omeprazole/pantaprazole), and H2 receptor antagonists (ranitidine), and of course, antibiotics and pain medication, and care for the incision site.

http://img2.tfd.com/mk/I/X2604-I-26.png

Don't know what currant jelly is?  

http://www.dansukker.co.uk/files/Billeder/recipe_large/currant_jelly.jpg

Yum.

Look, there's a million things we could cover, but things you really need to just know, VS, and that 1g=1mL of body fluid.  A loss of 1kg=1000mL fluid loss, and that's a problem when you're a tiny person.

Coronary Artery Oxygenation

"Myocardial Blood Flow-Coronary Vessels" by elcheguevarra

https://www.youtube.com/watch?v=tBQa8IBzP6I