random fact throwing: PCCN/CCRN edition

turnforthenurse, MSN, NP · Nov 3, 2012

Anyone? :) I plan on contributing more information soon...

turnforthenurse, MSN, NP · Nov 3, 2012

systolic HF: pump problem, because in systole, the heart contracts and this is what is failing. You'll see an EF of

diastolic HF: filling problem, because in diastole, the heart is supposed to relax and fill. In DHF, the heart is stiff and cannot relax.

Natrecor/niseritide

- synthetic BNP

- increases urine output by increasing GFR

- causes calcium to be more readily available = positive inotrope!

NEW S3 = fluid overload. suspect HF.

NEW S4 = stiff, non-compliant ventricle. suspect MI.

Dilated Cardiomyopathy (DCM) - most common

- atria are ALL STRETCHED OUT therefore you are more likely to see atrial fibrillation with this type of cardiomyopathy.

Hypertrophic Cardiomyopathy (HCM) - rare. genetic predisposition.

- tight outflow tract

- a decrease in volume or increase in outward force can cause the septum to fall on an outflow tract -> no blood leaving the heart -> sudden cardiac death!

- no diuretics or positive inotropes for the reason mentioned above.

Restrictive Cardiomyopathy (RCM)

- fibrous changes in the heart -> non-compliant. Does not fill, stretch or contract well.

SummitRN, BSN, RN · Nov 4, 2012

I like this. My learning style retains random facts well and integrates them into concepts and actionable information.

turnforthenurse, MSN, NP · Nov 6, 2012

Beck's Triad (cardiac tamponade) - the three D's

1. distant (muffled) heart sounds - because there is an accumulation of fluid in the pericardial sac

2. decreased (narrowed) pulse pressure - SBP drops because of decreased cardiac output and DBP rises due to decreased filling time

3. jugular vein distention (JVD)

may see electrical alternans with late or rapid tamponade (beat to beat differences in QRS amplitude)

pulsus paradoxus (>10mm Hg drop in SBP during inspiration)

Aortic Aneurysms: severe tearing, ripping-like pain not relieved with analgesics

BP/pulse differences between arms and legs

acute aortic valve insuffiency: high-pitched blowing, diastolic murmur that sounds like a washing machine! very loud.

nipride is NOT a first choice treatment because it can cause rebound tachycardia.

descending AA: typically treated medically because surgical intervention has a very high mortality rate. requires cross-clamping of the aorta.

ascending AA: patient needs to go to the OR STAT.

Typically surgical repair is warranted if there is a dilation of >5cm.

HTN urgency: DBP >120mm Hg WITHOUT end organ damage

HTN emergency: DBP >120 WITH organ damage.

Goal: decrease MAP by at least 25% in 2 hours then to

sodium nitroprusside (Nipride) is the first choice agent. Mixed arterial/venous vasodilator.

Hydralazine: arterial vasodilator

Nicardipine: mixed arterial/venous vasodilator

Esmolol: cardio-selective beta blocker.

Labetalol: alpha-blocker, NON-cardioselective beta blocker.

diuretics can WORSEN HTN by causing pressure-induced natriuresis (stimulates vasoconstriction) ***'

ALI (ARDS) can result from direct or indirect lung injury. Direct could be smoke inhalation or aspiration. Indirect could be anything that mediates the inflammatory response (sepsis!)

With ALI, there is an overwhelming inflammatory process in the lung = increased permeability and capillary leak leading to fluid leaking into the pulmonary interstitium -> alveoli -> diffuse, non-cardiogenic pulmonary edema.

Virchow's Triad

1. Venous stasis

2. Hypercoagulability

3. Vascular wall damage

turnforthenurse, MSN, NP · Nov 10, 2012

The oxyhemoglobin dissociation curve affects AFFINITY of oxygen to hemoglobin. Left shift = LOCKED and is bad for the patient. Shift to the left is caused by:

* alkalosis

* hypothermia

* low 2-3 DPG (seen in low phosphorus levels, hypothyroidism and blood tranfusions...so check your phos levels and make sure they are within range!)

Left shift increases affinity between O2 and Hgb HOWEVER the O2 does not get delivered at the tissue level. O2 stays bound to hemoglobin. LEFT = LOCKED.

* H/H, SaO2 normal. ScVO2 is elevated (poor cellular O2 consumption)

DI (diabetes insipidus)

* excessive polyuria

* low USG (

* excessive dehydration

* high serum Na+ (remember dehydration = high Na+; overhydration = low Na+ due to dilution)

* DI = dehydration!

SIADH (syndrome of inappropriate ADH)

* oliguria (

* high USG (>1.030)

* low Na+ (dilutional)...can be severe, 120mEq/L

* decreased BUN (dilutional), serum Osmo

DKA: hyperglycemic crisis resulting in metabolic acidosis and ketosis (type 1 diabetics)

HHNKS: hyperglycemic crisis with ABSENCE OF metabolic acidosis and ketosis...in patients with a relative insulin deficiency (i.e. type 2 diabetics)

DKA:

* Serum glucose 300-800mg/dL

* normal serum Na+

* high serum K+ (d/t acidosis) that later becomes LOW once insulin is administered (insulin drives K+ back into the cell)

* Increased BUN/Cr

* increased serum osmo

* metabolic acidosis

HHNKS:

* Serum glucose >600-2000mg/dL

* LOW serum Na+ due to hyperglycemia

* LOW serum K+ (no acidosis)

* Elevated BUN/Cr

* Increased serum osmo (more so than in DKA patients)

* NO acidosis...if there is an acidosis, consider lactic acidosis.

Causes of metabolic acidosis:

* DKA/ETOH ketoacidosis

* renal failure

* lactic acidosis

* ASA overdose

I hear the test can go pretty in-depth in differentiating between DI/SIADH and DKA/HHNKS, especially in regards to electrolyte imbalances. Hopefully this helps!

turnforthenurse, MSN, NP · Nov 10, 2012

HIT: heparin-induced thrombocytopenia

* typically occurs 4-10 days after initiating heparin therapy

* acquired allergy to heparin

* see a drop in platelet count (~50% from baseline)

* some patients will develop thrombi, hence the name HITT (heparin-induced thrombocytopenia and thrombi)

* STOP ALL HEPARIN, including Lovenox!

TTP - thrombotic thrombocytopenic purpura

* patient is throwing clots....decrease in platelet count

* clinical presentation is typically neuro symptoms or renal dysfunction and fever

* usually drug-induced

* give patient platelets or Neumega

ITP - idiopathic thrombocytopenic purpura

* Plt

* idiopathic...speculated to be autoimmune

When there is a 50% drop in platelet count, consider:

1. sepsis (you will see a drop in platelet count in early sepsis)

2. DIC

3. HIT

DIC - disseminated intravascular coagulation

* secondary disorder resulting from a primary pathological state or disease

* microvascular thrombi and bleeding

* A lot of risk factors....

* tissue damage from major surgery, major trauma, head trauma, acidosis

* obstetrical complications such as fetal demise, HELLP, eclampsia

* shock

* neoplasms

* TTP, sickle cell crisis

* acute/chronic renal failure, ulcerative colitis, DKA, cirrhosis, acute pancreatitis, liver dysfunction/failure, SIRS/MODS, PE

Decreased H/H, Plt

Increased PT, PTT, bleeding time

Fibrinogen is decreased because it is all used up!

FDP/FSP increased

D-Dimer increased

Antithrombin III decreased

Cryoprecipitate has the clotting factors these patients need! May also give Heparin though controversial...Heparin is to stop the clotting which may stop the bleeding. Typically given in early DIC.

Whoever is reading this or studying for their PCCN/CCRN, feel free to contribute.... :)

Kitesurfing bum · Nov 16, 2012

I like your style. I'll throw down.

Surprising how many have difficulty distinguishing between these 2:

* Svo2: drawn from pulmonary artery. INCLUDES coronary sinus. GLOBAL. 60-80%

* Scvo2: drawn from SVC. Does NOT include coronaries. >70%

*Retroperitoneal hemorrhage:

Risk factors: percutaneous vascular access, anticoagulated, trauma, hemodialysis, or in my pts case the other day, back/spinal surgery.

S/S: back, groin, flank, lower abd pain. Decreased H&H. Mild hypotension and tachycardia. Abdominal compartment syndrome.

Treat: normalize coagulation factors, blood transfusion, fluid resuscitation. Last resort=open surgery to drain hematoma and find/repair bleed.

*NTG is the go to vasodilator for pre-eclampsia to prevent fetal abnormalities.

*Q: What should you do for a pt with chest pain, hypotension, tachycardia (say 180bpm)? A: sync cardioversion

More to come...

csweetooth · Feb 11, 2013

Thank you so much for this post. I started a 2 day PCCN review course at work. I feel like its NCLEX all over again. I welcome advice and more facts!!

Danielle_thompson84 · Mar 16, 2013

Great thread!

susan.milner · Apr 17, 2013

ABG's made easy;

you can be acidotic w/either too much acid (respiratory) or not enough base (metabolic)

you can be alkolotic w/either too much base (metabolic) or not enough acid (respiratory)

if your pH is normal and HcO3 or CO2 is out of wack, it's compensating

if your pH is out of not normal, you are not compensating; sort of, if it's attempting to correct (as evidenced by movement of HCO3 & CO2 towards normal), it's partially compensated.

Anyone still studying? I'm testing in May and need LOTS more help!!!!!!!!!!!!

rtx723 · Jul 9, 2013

This is helpful~!